{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Amrute JM"],"funding":["NHLBI NIH HHS","NCI NIH HHS","NIAMS NIH HHS"],"pubmed_abstract":["Inflammation and tissue fibrosis co-exist and are causally linked to organ dysfunction. However, the molecular mechanisms driving immune-fibroblast crosstalk in human cardiac disease remains unexplored and there are currently no therapeutics to target fibrosis. Here, we performed multi-omic single-cell gene expression, epitope mapping, and chromatin accessibility profiling in 38 donors, acutely infarcted, and chronically failing human hearts. We identified a disease-associated fibroblast trajectory marked by cell surface expression of fibroblast activator protein (FAP), which diverged into distinct myofibroblasts and pro-fibrotic fibroblast populations, the latter resembling matrifibrocytes. Pro-fibrotic fibroblasts were transcriptionally similar to cancer associated fibroblasts and expres"],"journal":["Research square"],"pagination":["rs.3.rs-2402606"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9900986"],"repository":["biostudies-literature"],"pubmed_title":["Targeting Immune-Fibroblast Crosstalk in Myocardial Infarction and Cardiac Fibrosis."],"pmcid":["PMC9900986"],"funding_grant_id":["P30 CA091842","P30 AR073752","R01 HL138466","R35 HL161185","R01 HL151078","R01 HL139714"],"pubmed_authors":["Ma P","Lee P","Heo GS","Kuppe C","Lavine KJ","Jones C","Bredemeyer A","Koenig AL","Liu Y","Li CM","Kadyrov F","Furtado M","Kramann R","Amrute JM","Ason B","Kreisel D","Penna V","Terada Y","Fu A","Stitziel NO","Yamawaki T","Luo X","Hayat S","Yang S","Kopecky B","Shi SY"],"additional_accession":[]},"is_claimable":false,"name":"Targeting Immune-Fibroblast Crosstalk in Myocardial Infarction and Cardiac Fibrosis.","description":"Inflammation and tissue fibrosis co-exist and are causally linked to organ dysfunction. However, the molecular mechanisms driving immune-fibroblast crosstalk in human cardiac disease remains unexplored and there are currently no therapeutics to target fibrosis. Here, we performed multi-omic single-cell gene expression, epitope mapping, and chromatin accessibility profiling in 38 donors, acutely infarcted, and chronically failing human hearts. We identified a disease-associated fibroblast trajectory marked by cell surface expression of fibroblast activator protein (FAP), which diverged into distinct myofibroblasts and pro-fibrotic fibroblast populations, the latter resembling matrifibrocytes. Pro-fibrotic fibroblasts were transcriptionally similar to cancer associated fibroblasts and expres","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2026-06-25T03:13:55.865Z","creation":"2026-06-25T03:07:51.782Z"},"accession":"S-EPMC9900986","cross_references":{"pubmed":["36747878"],"doi":["10.21203/rs.3.rs-2402606/v1"]}}