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Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.
Hardy, Sean A; Liesinger, Laura; Patrick, Ralph; Poettler, Maria; Rech, Lavinia; Gindlhuber, Juergen; Mabotuwana, Nishani S; Ashour, DiyaaEldin; Stangl, Verena; Bigland, Mark; Murtha, Lucy A; Starkey, Malcolm R; Scherr, Daniel; Hansbro, Philip M; Hoefler, Gerald; Campos Ramos, Gustavo; Cochain, Clement; Harvey, Richard P; Birner-Gruenberger, Ruth; Boyle, Andrew J; Rainer, Peter P.
Afiliação
  • Hardy SA; Department of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
  • Liesinger L; School of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.
  • Patrick R; Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia.
  • Poettler M; Diagnostic and Research Institute of Pathology, Medical University of Graz, Graz, Austria.
  • Rech L; Institute of Chemical Technologies and Analytical Chemistry, Technische Universität Wien, Vienna, Austria.
  • Gindlhuber J; School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, New South Wales, Australia.
  • Mabotuwana NS; St. Vincent's Clinical School, Faculty of Medicine, UNSW Sydney, Sydney, Australia.
  • Ashour D; Department of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
  • Stangl V; Department of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
  • Bigland M; Department of Cardiac Surgery, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
  • Murtha LA; Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
  • Starkey MR; Department of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
  • Scherr D; School of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.
  • Hansbro PM; Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia.
  • Hoefler G; Comprehensive Heart Failure Center, University Hospital Würzburg, Würzburg, Germany.
  • Campos Ramos G; Diagnostic and Research Institute of Pathology, Medical University of Graz, Graz, Austria.
  • Cochain C; School of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.
  • Harvey RP; Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia.
  • Birner-Gruenberger R; School of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.
  • Boyle AJ; Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia.
  • Rainer PP; Department of Immunology, Central Clinical School, Monash University, Melbourne, Victoria, Australia.
JACC Basic Transl Sci ; 8(12): 1539-1554, 2023 Dec.
Article em En | MEDLINE | ID: mdl-38205347
ABSTRACT
Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascular cells in uninjured human and mouse hearts, and from M1 and M2 macrophages and myofibroblasts after MI. ECM-1 stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic and inflammatory pathways, and inhibits cardiac fibroblast migration. ECM-1 binds HuCFb cell surface receptor LRP1, and LRP1 inhibition blocks ECM-1 from stimulating fibroblast-to-myofibroblast transition, confirming a novel ECM-1-LRP1 fibrotic signaling axis. ECM-1 may represent a novel mechanism facilitating inflammation-fibrosis crosstalk.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Áustria

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Áustria