study_acronym	study_internal	associated_study_acronyms	libraries	donors	LMX_ID	study_title	study_description	study_authors	publication_status	paper_reference	paper_link	PMID	DOI	pmid_source	accession	lungmap_url	paper_title	authors	journal	year	abstract	publication	page_description	source_accession	source_repository	source_pmid	source_doi	source_data_url	source_publication_url
Guo 2023 AJRCCM	ACDMPV	Guo 2023 AJRCCM (5 libraries)	5	5	LMEX0000004408	Alveolar capillary dysplasia with misalignment of the pulmonary veins (ACDMPV)	"ACDMPV is a lethal developmental disorder of lung morphogenesis caused by insufficiency of FOXF1 (forkhead box F1) transcription factor function. The cellular and transcriptional mechanisms by which FOXF1 deficiency disrupts human lung formation are unknown. To identify cell types, gene networks, and cell-cell interactions underlying the pathogenesis of ACDMPV. We used single-nucleus RNA and assay for transposase-accessible chromatin sequencing, immunofluorescence confocal microscopy, and RNA in situ hybridization to identify cell types and molecular networks influenced by FOXF1 in ACDMPV lungs. Pathogenic single-nucleotide variants and copy-number variant deletions involving the FOXF1 gene locus in all subjects with ACDMPV (n = 6) were accompanied by marked changes in lung structure, including deficient alveolar development and a paucity of pulmonary microvasculature. Single-nucleus RNA and assay for transposase-accessible chromatin sequencing identified alterations in cell number and gene expression in endothelial cells (ECs), pericytes, fibroblasts, and epithelial cells in ACDMPV lungs. Distinct cell-autonomous roles for FOXF1 in capillary ECs and pericytes were identified. Pathogenic variants involving the FOXF1 gene locus disrupt gene expression in EC progenitors, inhibiting the differentiation or survival of capillary 2 ECs and cell-cell interactions necessary for both pulmonary vasculogenesis and alveolar type 1 cell differentiation. Loss of the pulmonary microvasculature was associated with increased VEGFA (vascular endothelial growth factor A) signaling and marked expansion of systemic bronchial ECs expressing COL15A1 (collagen type XV α 1 chain). Distinct FOXF1 gene regulatory networks were identified in subsets of pulmonary endothelial and fibroblast progenitors, providing both cellular and molecular targets for the development of therapies for ACDMPV and other diffuse lung diseases of infancy."	"Minzhe Guo 1 , Kathryn A. Wikenheiser-Brokamp 1 , Joseph A. Kitzmiller 1 , Cheng Jiang 1 , Guolun Wang 1 , Allen Wang 2 , Sebastian Preissl 2 , Yifei Miao 1 , David B. Frank 3 , William J. Zacharias 1 , Xin Sun 2 , Yan Xu 1 , Mingxia Gu 1 , Pawel Stankiewicz 4 , Vladimir V. Kalinichenko 1 , Jennifer A. Wambach 5 , Jeffrey A. Whitsett 1 1 Cincinnati Children's Hospital Medical Center, 2 University of California, San Diego, 3 Children’s Hospital of Philadelphia, 4 Baylor College of Medicine, 5 Washington University School of Medicine, * Corresponding author"	published	"Guo, et al. (2023)"	https://doi.org/10.1164/rccm.202210-2015OC	37463497	10.1164/rccm.202210-2015OC	dataset title matches publication title		https://www.lungmap.net/dataset/?dataset_id=LMEX0000004408	Single Cell Multiomics Identifies Cells and Genetic Networks Underlying Alveolar Capillary Dysplasia.	Guo M; Wikenheiser-Brokamp KA; Kitzmiller JA; Jiang C; Wang G; Wang A; Preissl S; Hou X; Buchanan J; Karolak JA; Miao Y; Frank DB; Zacharias WJ; Sun X; Xu Y; Gu M; Stankiewicz P; Kalinichenko VV; Wambach JA; Whitsett JA	Am J Respir Crit Care Med	2023	"ACDMPV is a lethal developmental disorder of lung morphogenesis caused by insufficiency of FOXF1 (forkhead box F1) transcription factor function. The cellular and transcriptional mechanisms by which FOXF1 deficiency disrupts human lung formation are unknown. To identify cell types, gene networks, and cell-cell interactions underlying the pathogenesis of ACDMPV. We used single-nucleus RNA and assay for transposase-accessible chromatin sequencing, immunofluorescence confocal microscopy, and RNA in situ hybridization to identify cell types and molecular networks influenced by FOXF1 in ACDMPV lungs. Pathogenic single-nucleotide variants and copy-number variant deletions involving the FOXF1 gene locus in all subjects with ACDMPV (n = 6) were accompanied by marked changes in lung structure, including deficient alveolar development and a paucity of pulmonary microvasculature. Single-nucleus RNA and assay for transposase-accessible chromatin sequencing identified alterations in cell number and gene expression in endothelial cells (ECs), pericytes, fibroblasts, and epithelial cells in ACDMPV lungs. Distinct cell-autonomous roles for FOXF1 in capillary ECs and pericytes were identified. Pathogenic variants involving the FOXF1 gene locus disrupt gene expression in EC progenitors, inhibiting the differentiation or survival of capillary 2 ECs and cell-cell interactions necessary for both pulmonary vasculogenesis and alveolar type 1 cell differentiation. Loss of the pulmonary microvasculature was associated with increased VEGFA (vascular endothelial growth factor A) signaling and marked expansion of systemic bronchial ECs expressing COL15A1 (collagen type XV α 1 chain). Distinct FOXF1 gene regulatory networks were identified in subsets of pulmonary endothelial and fibroblast progenitors, providing both cellular and molecular targets for the development of therapies for ACDMPV and other diffuse lung diseases of infancy."		"ACDMPV is a lethal developmental disorder of lung morphogenesis caused by insufficiency of FOXF1 (forkhead box F1) transcription factor function. The cellular and transcriptional mechanisms by which FOXF1 deficiency disrupts human lung formation are unknown. To identify cell types, gene networks, and cell-cell interactions underlying the pathogenesis of ACDMPV. We used single-nucleus RNA and assay for transposase-accessible chromatin sequencing, immunofluorescence confocal microscopy, and RNA in situ hybridization to identify cell types and molecular networks influenced by FOXF1 in ACDMPV lungs. Pathogenic single-nucleotide variants and copy-number variant deletions involving the FOXF1 gene locus in all subjects with ACDMPV (n = 6) were accompanied by marked changes in lung structure, including deficient alveolar development and a paucity of pulmonary microvasculature. Single-nucleus RNA and assay for transposase-accessible chromatin sequencing identified alterations in cell number and gene expression in endothelial cells (ECs), pericytes, fibroblasts, and epithelial cells in ACDMPV lungs. Distinct cell-autonomous roles for FOXF1 in capillary ECs and pericytes were identified. Pathogenic variants involving the FOXF1 gene locus disrupt gene expression in EC progenitors, inhibiting the differentiation or survival of capillary 2 ECs and cell-cell interactions necessary for both pulmonary vasculogenesis and alveolar type 1 cell differentiation. Loss of the pulmonary microvasculature was associated with increased VEGFA (vascular endothelial growth factor A) signaling and marked expansion of systemic bronchial ECs expressing COL15A1 (collagen type XV α 1 chain). Distinct FOXF1 gene regulatory networks were identified in subsets of pulmonary endothelial and fibroblast progenitors, providing both cellular and molecular targets for the development of therapies for ACDMPV and other diffuse lung diseases of infancy."	LMEX0000004408	LungMAP	37463497	10.1164/rccm.202210-2015OC	https://data-browser.lungmap.net/projects/fdadee7e-2097-45d5-bf81-cc280bd8348e	https://pubmed.ncbi.nlm.nih.gov/37463497/
Adams 2020 SciAdv	Adams	Adams 2020 SciAdv (78 libraries)	78	78	LMEX0000004393	Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis	Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis	"Naftali Kaminski 1 , Ivan O. Rosas 2 , Taylor S. Adams 1 , Jonas C. Schupp 1 , Sergio Poli 2 1 Yale School of Medicine, 2 Harvard Medical School, * Corresponding author"	published	Adams et al. (2020)	https://pubmed.ncbi.nlm.nih.gov/32832599/	32832599	10.1126/sciadv.aba1983	breath experiment_publication link	GSE136831	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004393	Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis.	Adams TS; Schupp JC; Poli S; Ayaub EA; Neumark N; Ahangari F; Chu SG; Raby BA; DeIuliis G; Januszyk M; Duan Q; Arnett HA; Siddiqui A; Washko GR; Homer R; Yan X; Rosas IO; Kaminski N	Sci Adv	2020	Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis	Adams et al. (2020)	Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis	GSE136831	NCBI GEO	32832599	10.1126/sciadv.aba1983	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136831	https://pubmed.ncbi.nlm.nih.gov/32832599/
Perl 2026 LungMAP	BOS	Perl 2026 LungMAP (5 libraries)	5	1	LMEX0000004409	Bronchiolitis Obliterans Syndrome Airway scRNA-Seq	"In as many as half of all lung transplant patients, Bronchiolitis Obliterans Syndrome or BOS, can develop, resulting in a progress deterioration of lung function. In this experiment, scRNA-Seq was performed on a series of 5 distal and proximal airway regions of the removed lung, prior to transplantation. The patient was a a male 9 year old, with BOS confirmed upon biopsy, which occurred after a bone marrow transplantation (graft versus host rejection). The sample was prepared from flash frozen sample, processed using a cold activated protease protocol in the laboratory of Anne Karina Perl (Cincinnati Children's Hospital - IRB 2013-3309). The dataset was processed using the Terra Optimus and Cumulus pipelines to produce unsupervised louvain clusters as well as in the software ICGS2 (unsupervised) and cellHarmony (supervised) to identify cell population identities relative to prior published studies."	"Anne Karina Perl 1 1 Cincinnati Children's Hospital Medical Center, * Corresponding author"	unpublished; cite the LungMAP dataset		https://www.lungmap.net/dataset/?dataset_id=LMEX0000004409					https://www.lungmap.net/dataset/?dataset_id=LMEX0000004409					"In as many as half of all lung transplant patients, Bronchiolitis Obliterans Syndrome or BOS, can develop, resulting in a progress deterioration of lung function. In this experiment, scRNA-Seq was performed on a series of 5 distal and proximal airway regions of the removed lung, prior to transplantation. The patient was a a male 9 year old, with BOS confirmed upon biopsy, which occurred after a bone marrow transplantation (graft versus host rejection). The sample was prepared from flash frozen sample, processed using a cold activated protease protocol in the laboratory of Anne Karina Perl (Cincinnati Children's Hospital - IRB 2013-3309). The dataset was processed using the Terra Optimus and Cumulus pipelines to produce unsupervised louvain clusters as well as in the software ICGS2 (unsupervised) and cellHarmony (supervised) to identify cell population identities relative to prior published studies."		"In as many as half of all lung transplant patients, Bronchiolitis Obliterans Syndrome or BOS, can develop, resulting in a progress deterioration of lung function. In this experiment, scRNA-Seq was performed on a series of 5 distal and proximal airway regions of the removed lung, prior to transplantation. The patient was a a male 9 year old, with BOS confirmed upon biopsy, which occurred after a bone marrow transplantation (graft versus host rejection). The sample was prepared from flash frozen sample, processed using a cold activated protease protocol in the laboratory of Anne Karina Perl (Cincinnati Children's Hospital - IRB 2013-3309). The dataset was processed using the Terra Optimus and Cumulus pipelines to produce unsupervised louvain clusters as well as in the software ICGS2 (unsupervised) and cellHarmony (supervised) to identify cell population identities relative to prior published studies."	LMEX0000004409	LungMAP / Broad Single Cell Portal			https://data-browser.lungmap.net/projects/4ae8c5c9-1520-4371-9827-6935661f6c84	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004409
Sun 2026 LungMAP	BPD	Sun 2026 LungMAP (42 libraries)	42	24	LMEX0000004400	Bronchopulmonary Dysplasia (BPD) — LungMAP/Xin Sun	"Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by alveolar dysplasia in newborns that are typically born prematurely. In this study, single-nucleus RNA-Sequencing was performed on BPD infants (n=13) and age matched controls (n=11) who died from complications associated with BPD (4 months to 3 years of age)."	"Xin Sun 1 , Gloria Pryhuber 2 , Allen Wang 1 1 University of California, San Diego, 2 University of Rochester Medical Center, * Corresponding author"	unpublished; cite the LungMAP dataset		https://www.lungmap.net/dataset/?dataset_id=LMEX0000004400					https://www.lungmap.net/dataset/?dataset_id=LMEX0000004400					"Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by alveolar dysplasia in newborns that are typically born prematurely. In this study, single-nucleus RNA-Sequencing was performed on BDPD infants (n=13) and age matched controls (n=11) who died from complications associated with BPD (4 months to 3 years of age)."		"Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by alveolar dysplasia in newborns that are typically born prematurely. In this study, single-nucleus RNA-Sequencing was performed on BDPD infants (n=13) and age matched controls (n=11) who died from complications associated with BPD (4 months to 3 years of age)."	LMEX0000004400	LungMAP			https://data-browser.lungmap.net/projects/1977dc47-8414-4263-a870-6b0f207d8ab3	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004400
Basil 2022 Nature	Basil-2022	Basil 2022 Nature (18 libraries)	18	9	LMEX0000004405	Respiratory Airway Secretory Cells in COPD	"The human lung differs substantially from its murine counterpart, resulting in a distinct distal airway architecture affected by disease pathology in chronic obstructive pulmonary disease. In humans, the distal branches of the airway interweave with the alveolar gas exchange niche, forming an anatomical structure known as the respiratory bronchioles. Due to the lack of a murine counterpart, the cellular and molecular characterization of these respiratory bronchioles in the human lung remains an enigma. We show that human respiratory bronchioles contain a unique secretory cell population that is distinct from cells in larger proximal airways. Organoid modeling reveals that these respiratory airway secretory cells (RASCs) act as unidirectional progenitors for alveolar type 2 cells, which are essential for maintaining and regenerating the alveolar niche. RASC lineage differentiation into AT2 cells is regulated by Notch and Wnt signaling. In COPD, RASCs are altered transcriptionally, corresponding to abnormal AT2 cell states, which are associated with smoking exposure in both humans and ferrets. These data identify a distinct progenitor in a region of the human lung not found in mouse that plays a critical role in maintaining the gas exchange compartment and is altered in chronic lung disease."	"Maria C. Basil 1 , Fabian L. Cardenas-Diaz 1 , Jaymin J. Kathiriya 2 , Michael P. Morley 1 , Justine Carl 1 , Alexis N. Brumwell 2 , Jeremy Katzen 1 , Katherine J. Slovik 1 , Apoorva Babu 3 , Su Zhou 1 , Madison M. Kremp 1 , Katherine B. McCauley 4 , Shanru Li 1 , Joseph D. Planer 1 , Shah S. Hussain 5 , Xiaoming Liu 6 , Rebecca Windmueller 7 , Yun Ying 1 , Kathleen M. Stewart 1 , Michelle Oyster 1 , Jason D. Christie 1 , Joshua M. Diamond 1 , John F. Engelhardt 6 , Edward Cantu 3 , Steven M. Rowe 5 , Darrell N. Kotton 4 , Harold A. Chapman 2 , Edward E. Morrisey 1 1 Perelman School of Medicine, University of Pennsylvania, 2 University of California, San Francisco, 3 Penn-Children’s Hospital of Philadelphia Lung Biology Institute, 4 Boston University, 5 University of Alabama at Birmingham, 6 University of Iowa, 7 Children’s Hospital of Philadelphia, * Corresponding author"	published	Basil et al. (2022)	https://doi.org/10.1038/s41586-022-04552-0	35355013	10.1038/s41586-022-04552-0		GSE168191	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004405	Human distal airways contain a multipotent secretory cell that can regenerate alveoli		Nature	2022	"The human lung differs substantially from its murine counterpart, resulting in a distinct distal airway architecture affected by disease pathology in chronic obstructive pulmonary disease. In humans, the distal branches of the airway interweave with the alveolar gas exchange niche, forming an anatomical structure known as the respiratory bronchioles. Due to the lack of a murine counterpart, the cellular and molecular characterization of these respiratory bronchioles in the human lung remains an enigma. We show that human respiratory bronchioles contain a unique secretory cell population that is distinct from cells in larger proximal airways. Organoid modeling reveals that these respiratory airway secretory cells (RASCs) act as unidirectional progenitors for alveolar type 2 cells, which are essential for maintaining and regenerating the alveolar niche. RASC lineage differentiation into AT2 cells is regulated by Notch and Wnt signaling. In COPD, RASCs are altered transcriptionally, corresponding to abnormal AT2 cell states, which are associated with smoking exposure in both humans and ferrets. These data identify a distinct progenitor in a region of the human lung not found in mouse that plays a critical role in maintaining the gas exchange compartment and is altered in chronic lung disease."		"The human lung differs substantially from its murine counterpart, resulting in a distinct distal airway architecture affected by disease pathology in chronic obstructive pulmonary disease. In humans, the distal branches of the airway interweave with the alveolar gas exchange niche, forming an anatomical structure known as the respiratory bronchioles. Due to the lack of a murine counterpart, the cellular and molecular characterization of these respiratory bronchioles in the human lung remains an enigma. We show that human respiratory bronchioles contain a unique secretory cell population that is distinct from cells in larger proximal airways. Organoid modeling reveals that these respiratory airway secretory cells (RASCs) act as unidirectional progenitors for alveolar type 2 cells, which are essential for maintaining and regenerating the alveolar niche. RASC lineage differentiation into AT2 cells is regulated by Notch and Wnt signaling. In COPD, RASCs are altered transcriptionally, corresponding to abnormal AT2 cell states, which are associated with smoking exposure in both humans and ferrets. These data identify a distinct progenitor in a region of the human lung not found in mouse that plays a critical role in maintaining the gas exchange compartment and is altered in chronic lung disease."	GSE168191	NCBI GEO	35355013	10.1038/s41586-022-04552-0	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE168191	https://pubmed.ncbi.nlm.nih.gov/35355013/
Zhang 2026 NatGenet	COPD-full	Zhang 2026 NatGenet (148 libraries)	148	141	LMEX0000009416	Aberrant cellular communities underlying disease heterogeneity in chronic obstructive pulmonary disease	"To investigate COPD heterogeneity, we profiled lung tissue by single-nucleus RNA sequencing from 141 study participants (1,516,727 nuclei) and identified shifts in cell composition and emergent cell states that correlated with lung function, emphysema and composite symptom scores. Epithelial regenerative states peaked in early COPD and declined thereafter, whereas inflamed nonimmune cells and profibrotic/remodeling states, together with select immune populations, expanded with disease progression. Clustering study participants by the proportion of pathologic cells coupled with spatial transcriptomics identified distinct patterns of cellular co-occurrence within spatially localized niches. Proteomic analyses identified plasma biomarkers of cell states and their impact on the extracellular matrix. Mediation and cell communication analyses revealed cell-autonomous and intercellular communication networks associated with disease. The data released here are metacells rather than individual nuclei: each metacell sums the counts of cells from two metadata-matched donors, and every metacell belongs to one of 178 meta-samples formed from 2 or 3 such donors. Clinical values are reported only as aggregates over those donor groups, so no released record corresponds to a single participant."	"Yuening Zhang 1 , Huanhuan Wei 1 , Jessica Nouws 1 , Wenhao Jiang 1 , Reginald M Brewster 1 , Jenny P Nguyen 1 , SiRu Liang 1 , Samuel M Pass 1 , Weiwei Wang , Florine Collin , Angela Taravella Oill 2 , Sang-Hun Kim 1 , Saul S Siller 1 , Jinjiang Liu , Amy Y Zhao 1 , Phillip Hansbro , Charles Dela Cruz , Clemente Britto 1 , Jose Gomez 1 , Suzanne M Cloonan , Erica L Herzog 1 , TuKiet T Lam 2 , Nicholas E. Banovich 2 , Micha Sam B Raredon 1 , Xuchen Zhang 1 , Stefano Mangiola 3 , Robert J Homer 1 , Naftali Kaminski 1 , John McDonough , Francesca Polverino 4 , Xiting Yan 1 , Maor Sauler 1 1 Yale School of Medicine, 2 Translational Genomics Research Institute, 3 University of Melbourne, 4 Baylor College of Medicine, * Corresponding author"	published	Aberrant cellular communities underlying disease heterogeneity in chronic obstructive pulmonary disease. Nature Genetics (2026). https://www.nature.com/articles/s41588-025-02480-z	https://pubmed.ncbi.nlm.nih.gov/41578022/	41578022	10.1038/s41588-025-02480-z	dataset title matches publication title	GSE310058	https://www.lungmap.net/dataset/?dataset_id=LMEX0000009416	Aberrant cellular communities underlying disease heterogeneity in chronic obstructive pulmonary disease.	Zhang Y; Wei H; Nouws J; Jiang W; Brewster RM; Nguyen JP; Liang S; Pass SM; Wang W; Collin F; Oill AT; Kim SH; Siller SS; Liu J; Zhao AY; Hansbro P; Dela Cruz C; Britto C; Gomez J; Cloonan SM; Herzog EL; Lam TT; Banovich NE; Raredon MSB; Zhang X; Mangiola S; Homer RJ; Kaminski N; McDonough J; Polverino F; Yan X; Sauler M	Nat Genet	2026	"To investigate COPD heterogeneity, we profiled lung tissue by single-nucleus RNA sequencing from 141 study participants (1,516,727 nuclei) and identified shifts in cell composition and emergent cell states that correlated with lung function, emphysema and composite symptom scores. Epithelial regenerative states peaked in early COPD and declined thereafter, whereas inflamed nonimmune cells and profibrotic/remodeling states, together with select immune populations, expanded with disease progression. Clustering study participants by the proportion of pathologic cells coupled with spatial transcriptomics identified distinct patterns of cellular co-occurrence within spatially localized niches. Proteomic analyses identified plasma biomarkers of cell states and their impact on the extracellular matrix. Mediation and cell communication analyses revealed cell-autonomous and intercellular communication networks associated with disease. The data released here are metacells rather than individual nuclei: each metacell sums the counts of cells from two metadata-matched donors, and every metacell belongs to one of 178 meta-samples formed from 2 or 3 such donors. Clinical values are reported only as aggregates over those donor groups, so no released record corresponds to a single participant."	Aberrant cellular communities underlying disease heterogeneity in chronic obstructive pulmonary disease. Nature Genetics (2025). https://www.nature.com/articles/s41588-025-02480-z	"To investigate COPD heterogeneity, we profiled lung tissue by single-nucleus RNA sequencing from 141 study participants (1,516,727 nuclei) and identified shifts in cell composition and emergent cell states that correlated with lung function, emphysema and composite symptom scores. Epithelial regenerative states peaked in early COPD and declined thereafter, whereas inflamed nonimmune cells and profibrotic/remodeling states, together with select immune populations, expanded with disease progression. Clustering study participants by the proportion of pathologic cells coupled with spatial transcriptomics identified distinct patterns of cellular co-occurrence within spatially localized niches. Proteomic analyses identified plasma biomarkers of cell states and their impact on the extracellular matrix. Mediation and cell communication analyses revealed cell-autonomous and intercellular communication networks associated with disease. The data released here are metacells rather than individual nuclei: each metacell sums the counts of cells from two metadata-matched donors, and every metacell belongs to one of 178 meta-samples formed from 2 or 3 such donors. Clinical values are reported only as aggregates over those donor groups, so no released record corresponds to a single participant."	GSE310058	NCBI GEO	41578022	10.1038/s41588-025-02480-z	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE310058	https://pubmed.ncbi.nlm.nih.gov/41578022/
Deutsch 2026 LungMAP	COVID-URMC	Deutsch 2026 LungMAP (52 libraries)	52	50	LMEX0000004406	CITE-Seq of COVID-19 Human Lungs	"Single-cell CITE-Seq of human COVID-19 infected and control lungs, spanning lifespan, using an optimized protocol for 10X Genomics Single Cell 3' (v3.1) CITE-Seq analysis. This protocol describes the steps necessary for preparing generating sequencing data following staining single cells with ADT-tagged antibodies (including library preparation, sequencing steps, and mapping steps)."	"Gail H. Deutsch 1 , Ravi Misra 2 , Thomas J. Mariani 2 , Gloria Pryhuber 2 1 University of Washington, 2 University of Rochester Medical Center, * Corresponding author"	unpublished; cite the LungMAP dataset		https://www.lungmap.net/dataset/?dataset_id=LMEX0000004406					https://www.lungmap.net/dataset/?dataset_id=LMEX0000004406					"Single-cell CITE-Seq of human COVID-19 infected and control lungs, spanning lifespan, using an optimized protocol for  10X Genomics Single Cell 3' (v3.1) CITE-Seq analysis. This protocol describes the steps necessary for preparing generating sequencing data following staining single cells with ADT-tagged antibodies (including library preparation, sequencing steps, and mapping steps)."		"Single-cell CITE-Seq of human COVID-19 infected and control lungs, spanning lifespan, using an optimized protocol for 10X Genomics Single Cell 3' (v3.1) CITE-Seq analysis. This protocol describes the steps necessary for preparing generating sequencing data following staining single cells with ADT-tagged antibodies (including library preparation, sequencing steps, and mapping steps)."	LMEX0000004406	LungMAP			https://data-browser.lungmap.net/projects/834e0d16-71b6-4425-a8ab-022b5000961c	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004406
Olatoke 2023 SciAdv	LAM	Olatoke 2023 SciAdv (2 libraries)	2	2	LMEX0000004412	Single-cell multiome analysis of lymphangioleiomyomatosis (LAM)	Single-cell RNAseq of lymphangioleiomyomatosis (LAM) lungs to construct gene regulatory network controlling the transcriptional program of LAM cells. In vivo and in vitro LAM models were used to identify molecular mechanisms mediating LAM cell pathogenesis. Integrative single cell omics analyses identified the activation of uterine specific HOX-PBX transcriptional programs in pulmonary LAMCORE cells.	"Tasnim F. Olatoke 1 , Andrew Wagner 2 , Aristotelis A. Astrinidis 1 , Francis X. McCormack 1 , Yan Xu 2 , Jane J. Yu 1 1 University of Cincinnati College of Medicine, 2 Cincinnati Children's Hospital Medical Center, * Corresponding author"	published	Olatoke et al. (2023)	https://doi.org/10.1126/sciadv.adf8549	37163604	10.1126/sciadv.adf8549		GSE217107	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004412	Single-cell multiomic analysis identifies a HOX-PBX gene network regulating the survival of lymphangioleiomyomatosis cells		Sci Adv	2023	Single-cell RNAseq of lymphangioleiomyomatosis (LAM) lungs to construct gene regulatory network controlling the transcriptional program of LAM cells. In vivo and in vitro LAM models were used to identify molecular mechanisms mediating LAM cell pathogenesis. Integrative single cell omics analyses identified the activation of uterine specific HOX-PBX transcriptional programs in pulmonary LAMCORE cells.		Single-cell RNAseq of lymphangioleiomyomatosis (LAM) lungs to construct gene regulatory network controlling the transcriptional program of LAM cells. In vivo and in vitro LAM models were used to identify molecular mechanisms mediating LAM cell pathogenesis. Integrative single cell omics analyses identified the activation of uterine specific HOX-PBX transcriptional programs in pulmonary LAMCORE cells.	GSE217107	NCBI GEO	37163604	10.1126/sciadv.adf8549	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE217108	https://pubmed.ncbi.nlm.nih.gov/37163604/
Jaiswal 2026 CellGenom	MGH-ILD	Jaiswal 2026 CellGenom (40 libraries)	40	18		Spatial transcriptomics reveals altered communities and drivers of aberrant epithelia and pro-fibrotic fibroblasts in interstitial lung diseases.	"Interstitial lung diseases (ILD) are characterized by fibrotic scarring of the lung parenchyma with remarkably unfavorable prognosis. Using single-nucleus RNA sequencing and spatial transcriptomics, we generated a comprehensive cellular network of the distal lung and its alterations in fibrosis. Integration with histopathology revealed that the transformation of normal parenchyma into fibrotic tissue is accompanied by ectopic bronchiolization and decellularization. Areas of active fibrosis were characterized by co-localization of pro-fibrotic CTHRC1-hi fibroblasts and aberrant transitional epithelial cells. We modeled this maladaptive differentiation of alveolar epithelial cells using organoids, demonstrating that all three pro-inflammatory ligands present in this pathogenic niche, TGF-β, IL-1β, and TNF-α, are jointly required for their induction. Additionally, we identified a requirement for the transcription factor NFATC4 during myofibroblast differentiation driven by soluble factors or mechanosensing. Collectively, this work identifies essential molecular drivers of the cellular interactions underlying lung fibrosis."	Jaiswal A; Kooistra T; Pokatayev V; Bastos HN; Santos RF; Sarraf TR; Segerstolpe Å; Lin C; Amir-Zilberstein L; Twardus S; Shannon K; Murphy SP; Knipe R; Ganzleben IK; Black KE; Delorey TM; Graham DB; Hung YP; Hariri LP; Deguine J; Carvalho A; Medoff BD; Xavier RJ	published	Jaiswal et al. (2026) Cell Genomics	https://www.ncbi.nlm.nih.gov/pubmed/41576947	41576947	10.1016/j.xgen.2025.101066	"LungMAP publication list; cohort matches mmc2 (MGH 28, HSJ 15)"			Spatial transcriptomics reveals altered communities and drivers of aberrant epithelia and pro-fibrotic fibroblasts in interstitial lung diseases.	Jaiswal A; Kooistra T; Pokatayev V; Bastos HN; Santos RF; Sarraf TR; Segerstolpe Å; Lin C; Amir-Zilberstein L; Twardus S; Shannon K; Murphy SP; Knipe R; Ganzleben IK; Black KE; Delorey TM; Graham DB; Hung YP; Hariri LP; Deguine J; Carvalho A; Medoff BD; Xavier RJ	Cell Genom	2026				Cell Genomics supplementary table mmc2	Cell Genomics	41576947	10.1016/j.xgen.2025.101066	https://doi.org/10.1016/j.xgen.2025.101066	https://pubmed.ncbi.nlm.nih.gov/41576947/
Natri 2024 NatGenet	Natri-2024	Natri 2024 NatGenet (127 libraries)	127	92	LMEX0000004403	Single-cell RNA-seq analysis of Interstitial Lung Disease (ILD) subtypes	"ScRNA-seq profiles for 114 individuals, including 66 (58%) with ILD and 48 (42%) unaffected donors. The ILD lungs included samples from 39 individuals with IPF and 27 with other forms of pulmonary fibrosis, including sarcoidosis (n = 4), connective tissue disease-associated ILD (n = 3), idiopathic nonspecific interstitial pneumonia (n = 3), coal worker’s pneumoconiosis (n = 3), chronic hypersensitivity pneumonitis (n = 2), interstitial pneumonia with autoimmune features (n = 2) and unclassifiable ILD (n = 10). Most (67%) the lung samples were from individuals with self-reported ethnicity of European ancestry; 53 (46%) reported past or present tobacco use."	"Jonathan A. Kropski 1 , Nicholas E. Banovich 2 1 Vanderbilt University Medical Center, 2 Translational Genomics Research Institute, * Corresponding author"	published	"Natri, et al. (2024)"	https://doi.org/10.1038/s41588-024-01702-0	38548990	10.1038/s41588-024-01702-0		GSE227136; phs003521.v1.p1	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004403	Cell-type-specific and disease-associated expression quantitative trait loci in the human lung		Nat Genet	2024	"scRNA-seq profiles for 114 individuals, including 66 (58%) with ILD and 48 (42%) unaffected donors. The ILD lungs included samples from 39 individuals with IPF and 27 with other forms of pulmonary fibrosis, including sarcoidosis (n = 4), connective tissue disease-associated ILD (n = 3), idiopathic nonspecific interstitial pneumonia (n = 3), coal worker’s pneumoconiosis (n = 3), chronic hypersensitivity pneumonitis (n = 2), interstitial pneumonia with autoimmune features (n = 2) and unclassifiable ILD (n = 10). Most (67%) the lung samples were from individuals with self-reported ethnicity of European ancestry; 53 (46%) reported past or present tobacco use."		"ScRNA-seq profiles for 114 individuals, including 66 (58%) with ILD and 48 (42%) unaffected donors. The ILD lungs included samples from 39 individuals with IPF and 27 with other forms of pulmonary fibrosis, including sarcoidosis (n = 4), connective tissue disease-associated ILD (n = 3), idiopathic nonspecific interstitial pneumonia (n = 3), coal worker’s pneumoconiosis (n = 3), chronic hypersensitivity pneumonitis (n = 2), interstitial pneumonia with autoimmune features (n = 2) and unclassifiable ILD (n = 10). Most (67%) the lung samples were from individuals with self-reported ethnicity of European ancestry; 53 (46%) reported past or present tobacco use."	GSE227136; phs003521.v1.p1	NCBI GEO	38548990	10.1038/s41588-024-01702-0	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE227136	https://pubmed.ncbi.nlm.nih.gov/38548990/
Uehara 2023 NatCommun	PAM	Uehara 2023 NatCommun (1 libraries)	1	1	LMEX0000004361	Normal donor control from the pulmonary alveolar microlithiasis (PAM) study	D071 is the normal donor control in the PAM study.		published	Uehara et al. (2023)	https://pubmed.ncbi.nlm.nih.gov/36864068/	36864068	10.1038/s41467-023-36810-8		GSE199329	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004361	Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis		Nat Commun	2023				GSE199329	NCBI GEO	36864068	10.1038/s41467-023-36810-8	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE199329	https://pubmed.ncbi.nlm.nih.gov/36864068/
Uehara 2023 NatCommun	PAM	Uehara 2023 NatCommun (2 libraries)	2	1	LMEX0000004407	Human pulmonary alveolar microlithiasis (PAM) scRNA-Seq with SLC34A2 (Npt2b) mutations	Pulmonary alveolar microlithiasis (PAM) is an autosomal recessive lung disease caused by a deficiency in the pulmonary epithelial Npt2b sodium-phosphate co-transporter that results in accumulation of phosphate and formation of hydroxyapatite microliths in the alveolar space. The single cell transcriptomic analysis of a PAM lung explant showing a robust osteoclast gene signature in alveolar monocytes and the finding that calcium phosphate microliths contain a rich protein and lipid matrix that includes bone resorbing osteoclast enzymes suggested a role for osteoclast-like cells in the defense against microliths.	"Yasuaki Uehara 1 , Yusuke Tanaka 1 , Shuyang Zhao 2 , Nikolaos M. Nikolaidis 1 , Lori B. Pitstick 1 , Huixing Wu 1 , Jane J. Yu 1 , Erik Zhang 1 , Yoshihiro Hasegawa 1 , John G. Noel 1 , Jason C. Gardner 1 , Elizabeth J. Kopras 1 , Wendy D. Haffey 1 , Kenneth D. Greis 1 , Jinbang Guo 2 , Jason C. Woods 2 , Kathryn A. Wikenheiser-Brokamp 2 , Jennifer Kyle 3 , Charles Ansong 3 , Steven L. Teitelbaum 4 , Yoshikazu Inoue 5 , Göksel Altinişik 6 , Yan Xu 2 , Francis X. McCormack 1 1 University of Cincinnati College of Medicine, 2 Cincinnati Children's Hospital Medical Center, 3 Pacific Northwest National Laboratory, 4 Washington University School of Medicine, 5 National Hospital Organization Kinki-Chuo Chest Medical Center, 6 Pamukkale University, * Corresponding author"	published	Uehara et al. (2023)	https://doi.org/10.1038/s41467-023-36810-8	36864068	10.1038/s41467-023-36810-8		GSE199329	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004407	Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis		Nat Commun	2023	Pulmonary alveolar microlithiasis (PAM) is an autosomal recessive lung disease caused by a deficiency in the pulmonary epithelial Npt2b sodium-phosphate co-transporter that results in accumulation of phosphate and formation of hydroxyapatite microliths in the alveolar space. The single cell transcriptomic analysis of a PAM lung explant showing a robust osteoclast gene signature in alveolar monocytes and the finding that calcium phosphate microliths contain a rich protein and lipid matrix that includes bone resorbing osteoclast enzymes suggested a role for osteoclast-like cells in the defense against microliths.		Pulmonary alveolar microlithiasis (PAM) is an autosomal recessive lung disease caused by a deficiency in the pulmonary epithelial Npt2b sodium-phosphate co-transporter that results in accumulation of phosphate and formation of hydroxyapatite microliths in the alveolar space. The single cell transcriptomic analysis of a PAM lung explant showing a robust osteoclast gene signature in alveolar monocytes and the finding that calcium phosphate microliths contain a rich protein and lipid matrix that includes bone resorbing osteoclast enzymes suggested a role for osteoclast-like cells in the defense against microliths.	GSE199329	NCBI GEO	36864068	10.1038/s41467-023-36810-8	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE199329	https://pubmed.ncbi.nlm.nih.gov/36864068/
Guo 2023 NatCommun	SMG	Guo 2023 NatCommun (5 libraries)	5	5	LMEX0000004396	Human CellCards Multi-Study CellRef 1.0 Atlas	"The ""LungMAP Human Lung CellRef"" atlas incorporates 48 well-defined lung cell types (CellCards) catalogued from diverse anatomic locations and stages of lung maturation. This atlas spans sc/snRNA-seq of 505,256 lung cells from 148 normal human lung samples from 104 donors from parenchyma, trachea, bonchi, bronchus SMG and small airway. This study includes 21 new lung samples. An accompanying R-shiny app (Azimuth) enables fast supervised annotation of user-provided single-cell RNA-Seq datasets (see below)."	"Minzhe Guo 1 , Geremy Clair 2 , Joshua N. Adkins 2 , Gloria Pryhuber 3 , Ravi Misra 3 , Bruce Aronow 1 , Timothy L. Tickle 4 , Nathan Salomonis 1 , Xin Sun 5 , Edward E. Morrisey 6 , Jeffrey A. Whitsett 1 , Yan Xu 1 1 Cincinnati Children's Hospital Medical Center, 2 Pacific Northwest National Laboratory, 3 University of Rochester Medical Center, 4 The Broad Institute, 5 University of California, San Diego, 6 Perelman School of Medicine, University of Pennsylvania, * Corresponding author"	published	Guo et al. (2023)	https://doi.org/10.1038/s41467-023-40173-5	37516747	10.1038/s41467-023-40173-5	dataset title matches publication title		https://www.lungmap.net/dataset/?dataset_id=LMEX0000004396	Guided construction of single cell reference for human and mouse lung.	Guo M; Morley MP; Jiang C; Wu Y; Li G; Du Y; Zhao S; Wagner A; Cakar AC; Kouril M; Jin K; Gaddis N; Kitzmiller JA; Stewart K; Basil MC; Lin SM; Ying Y; Babu A; Wikenheiser-Brokamp KA; Mun KS; Naren AP; Clair G; Adkins JN; Pryhuber GS; Misra RS; Aronow BJ; Tickle TL; Salomonis N; Sun X; Morrisey EE; Whitsett JA; NHLBI LungMAP Consortium; Xu Y	Nat Commun	2023	"The ""LungMAP Human Lung CellRef"" atlas incorporates 48 well-defined lung cell types (CellCards) catalogued from diverse anatomic locations and stages of lung maturation. This atlas spans sc/snRNA-seq of 505,256 lung cells from 148 normal human lung samples from 104 donors from parenchyma, trachea, bonchi, bronchus SMG and small airway. This study includes 21 new lung samples. An accompanying R-shiny app (Azimuth) enables fast supervised annotation of user-provided single-cell RNA-Seq datasets (see below)."	Guo et al. (2023)	"The ""LungMAP Human Lung CellRef"" atlas incorporates 48 well-defined lung cell types (CellCards) catalogued from diverse anatomic locations and stages of lung maturation. This atlas spans sc/snRNA-seq of 505,256 lung cells from 148 normal human lung samples from 104 donors from parenchyma, trachea, bonchi, bronchus SMG and small airway. This study includes 21 new lung samples. An accompanying R-shiny app (Azimuth) enables fast supervised annotation of user-provided single-cell RNA-Seq datasets (see below)."	LMEX0000004396	LungMAP	37516747	10.1038/s41467-023-40173-5	https://data-browser.lungmap.net/projects/0e2b2441-92a5-424c-bce1-abc13435686f	https://pubmed.ncbi.nlm.nih.gov/37516747/
Wang 2020 eLife	Sun-2020	Wang 2020 eLife (9 libraries)	9	9	LMEX0000004388	"Single cell transcriptomic signatures of normal human newborn, child and adult lungs"	"Single cell transcriptomic signatures of normal human newborn, child and adult lungs"	"Xin Sun 1 , Allen Wang 1 , Sebastian Preissl 1 , Kyle Gaulton 1 , Jamie Verheyden 1 , Minzhe Guo 2 , Ravi Misra 3 , Gloria Pryhuber 3 , Jeffrey A. Whitsett 2 , Yan Xu 2 1 University of California, San Diego, 2 Cincinnati Children's Hospital Medical Center, 3 University of Rochester Medical Center, * Corresponding author"	published	Wang et al. (2020)	https://pubmed.ncbi.nlm.nih.gov/33164753/	33164753	10.7554/eLife.62522	breath experiment_publication link	GSE161382 (scRNA-seq); GSE161383 (SuperSeries)	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004388	Single-cell multiomic profiling of human lungs reveals cell-type-specific and age-dynamic control of SARS-CoV2 host genes.	Wang A; Chiou J; Poirion OB; Buchanan J; Valdez MJ; Verheyden JM; Hou X; Kudtarkar P; Narendra S; Newsome JM; Guo M; Faddah DA; Zhang K; Young RE; Barr J; Sajti E; Misra R; Huyck H; Rogers L; Poole C; Whitsett JA; Pryhuber G; Xu Y; Gaulton KJ; Preissl S; Sun X; NHLBI LungMap Consortium	Elife	2020	"Single cell transcriptomic signatures of normal human newborn, child and adult lungs"	Wang et al. (2020)	"Single cell transcriptomic signatures of normal human newborn, child and adult lungs"	GSE161382 (scRNA-seq); GSE161383 (SuperSeries)	NCBI GEO	33164753	10.7554/eLife.62522	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161382	https://pubmed.ncbi.nlm.nih.gov/33164753/
Morrisey 2026 LungMAP	UPenn	Morrisey 2026 LungMAP (68 libraries)	68	54	LMEX0000004415	Human pediatric developmental epochs	"UPenn LungMAP single-cell lung cohort (68 libraries; 54 donors) spanning healthy and disease samples, ages 0-73 years; 10x 3' v2, 10x 3' v3; cell."	Edward E. Morrisey; Michael P. Morley; Maria C. Basil	unpublished	Human pediatric developmental epochs; LungMAP dataset (unpublished)	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004415				LMEX0000004415	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004415					"UPenn LungMAP single-cell lung cohort (68 libraries; 54 donors) spanning healthy and disease samples, ages 0-73 years; 10x 3' v2, 10x 3' v3; cell."			LMEX0000004415	LungMAP			https://www.lungmap.net/dataset/?dataset_id=LMEX0000004415	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004415
Mellors 2025 JCIInsight	UPenn	Mellors 2025 JCIInsight (13 libraries)	13	6	LMEX0000004415	Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome	"UPenn bronchiolitis obliterans syndrome cohort (13 libraries; 6 donors) including CLAD-BOS, cGVHD-BOS, and healthy controls; 10x 3' v3; cell."		published	"Mellors et al. (2025), JCI Insight"	https://pubmed.ncbi.nlm.nih.gov/40232854/	40232854	10.1172/jci.insight.176596		GSE290834	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004415	Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome		JCI Insight	2025	"UPenn bronchiolitis obliterans syndrome cohort (13 libraries; 6 donors) including CLAD-BOS, cGVHD-BOS, and healthy controls; 10x 3' v3; cell."	Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome	"UPenn bronchiolitis obliterans syndrome cohort (13 libraries; 6 donors) including CLAD-BOS, cGVHD-BOS, and healthy controls; 10x 3' v3; cell."	GSE290834	NCBI GEO	40232854	10.1172/jci.insight.176596	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE290834	https://pubmed.ncbi.nlm.nih.gov/40232854/
Guo 2023 NatCommun	UPenn	Guo 2023 NatCommun (39 libraries)	39	24	LMEX0000004415	LungMAP Human Lung CellRef (UPenn/CCHMC newly generated normal lung data)	"UPenn/CCHMC Human Lung CellRef cohort (39 libraries; 24 donors) used for reference construction, predominantly healthy lung samples; 10x 3' v2, 10x 3' v3; cell."	"Minzhe Guo 1 , Geremy Clair 2 , Joshua N. Adkins 2 , Gloria Pryhuber 3 , Ravi Misra 3 , Bruce Aronow 1 , Timothy L. Tickle 4 , Nathan Salomonis 1 , Xin Sun 5 , Edward E. Morrisey 6 , Jeffrey A. Whitsett 1 , Yan Xu 1 1 Cincinnati Children's Hospital Medical Center, 2 Pacific Northwest National Laboratory, 3 University of Rochester Medical Center, 4 The Broad Institute, 5 University of California, San Diego, 6 Perelman School of Medicine, University of Pennsylvania, * Corresponding author"	primary dataset unpublished; sample reused in publication	"Guo et al. (2023), Nature Communications"	https://pubmed.ncbi.nlm.nih.gov/37516747/	37516747	10.1038/s41467-023-40173-5		LMEX0000004396	https://www.lungmap.net/dataset/?dataset_id=LMEX0000004415	Guided construction of single cell reference for human and mouse lung	Guo M; Morley MP; Jiang C; Wu Y; Li G; Du Y; Zhao S; Wagner A; Cakar AC; Kouril M; Jin K; Gaddis N; Kitzmiller JA; Stewart K; Basil MC; Lin SM; Ying Y; Babu A; Wikenheiser-Brokamp KA; Mun KS; Naren AP; Clair G; Adkins JN; Pryhuber GS; Misra RS; Aronow BJ; Tickle TL; Salomonis N; Sun X; Morrisey EE; Whitsett JA; NHLBI LungMAP Consortium; Xu Y	Nature Communications	2023	"UPenn/CCHMC Human Lung CellRef cohort (39 libraries; 24 donors) used for reference construction, predominantly healthy lung samples; 10x 3' v2, 10x 3' v3; cell."	Guided construction of single cell reference for human and mouse lung	"UPenn/CCHMC Human Lung CellRef cohort (39 libraries; 24 donors) used for reference construction, predominantly healthy lung samples; 10x 3' v2, 10x 3' v3; cell."	LMEX0000004396	LungMAP	37516747	10.1038/s41467-023-40173-5	https://www.lungmap.net/omics/?experiment_id=LMEX0000004396	https://pubmed.ncbi.nlm.nih.gov/37516747/