{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Z"],"funding":["National Natural Science Foundation of China"],"pagination":["e04552"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12499418"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(37)"],"pubmed_abstract":["Progressive cardiac fibrosis post myocardial infarction (MI) drives pathological remodeling and heart failure, yet the role of endoplasmic reticulum-selective autophagy (ER-phagy) in this process remains unclear. Autocrine Motility Factor Receptor (AMFR) is a recently identified ER-phagy regulator, whose function under myocardial pathology remains poorly understood. Here, it is found that FAM134B-mediated ER-phagy activity is elevated in fibrotic mouse heart tissues post-MI and in cardiac fibroblasts stimulated by TGF-β1. AMFR knockout in mice aggravated cardiac fibrosis post-MI and worsened cardiac function, with scRNA-seq analysis demonstrating that AMFR-null cardiac fibroblasts exhibit a myofibroblast phenotype. Simultaneously, AMFR overexpression in cardiac fibroblasts reduces the expr"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["ER-phagy Activation by AMFR Attenuates Cardiac Fibrosis Post-Myocardial Infarction via mTORC1 Pathway."],"pmcid":["PMC12499418"],"funding_grant_id":["82271592"],"pubmed_authors":["Jin X","Li T","Niu K","Yang B","Chen Y","Lin Y","Wang X","Jin Y","Wang Z","Liu W"],"additional_accession":[]},"is_claimable":false,"name":"ER-phagy Activation by AMFR Attenuates Cardiac Fibrosis Post-Myocardial Infarction via mTORC1 Pathway.","description":"Progressive cardiac fibrosis post myocardial infarction (MI) drives pathological remodeling and heart failure, yet the role of endoplasmic reticulum-selective autophagy (ER-phagy) in this process remains unclear. Autocrine Motility Factor Receptor (AMFR) is a recently identified ER-phagy regulator, whose function under myocardial pathology remains poorly understood. Here, it is found that FAM134B-mediated ER-phagy activity is elevated in fibrotic mouse heart tissues post-MI and in cardiac fibroblasts stimulated by TGF-β1. AMFR knockout in mice aggravated cardiac fibrosis post-MI and worsened cardiac function, with scRNA-seq analysis demonstrating that AMFR-null cardiac fibroblasts exhibit a myofibroblast phenotype. Simultaneously, AMFR overexpression in cardiac fibroblasts reduces the expr","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-04T04:47:11.078Z","creation":"2026-05-05T03:12:39.014Z"},"accession":"S-EPMC12499418","cross_references":{"pubmed":["40673870"],"doi":["10.1002/advs.202504552"]}}