Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Hardy, SA; Liesinger, L; Patrick, R; Poettler, M; Rech, L; Gindlhuber, J; Mabotuwana, NS; Ashour, D; Stangl, V; Bigland, M; Murtha, LA; Starkey, MR; Scherr, D; Hansbro, PM; Hoefler, G; Campos, Ramos, G; Cochain, C; Harvey, RP; Birner-Gruenberger, R; Boyle, AJ; Rainer, PP.
Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.
JACC Basic Transl Sci. 2023; 8(12): 1539-1554.
Doi: 10.1016/j.jacbts.2023.05.010
[OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
- Rainer Peter
- Co-Autor*innen der Med Uni Graz
- Birner-Grünberger Ruth
- Gindlhuber Jürgen
- Höfler Gerald
- Liesinger Laura
- Rech Cara Lavinia Shirin
- Scherr Daniel
- Stangl Verena Maria
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- 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.
- Find related publications in this database (Keywords)
- extracellular matrix
- fibroblasts
- fibrosis
- heart
- inflammation
- myocardial infarction