Selected Publication:

SHR Neuro Cancer Cardio Lipid Metab 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

 

Leading authors Med Uni Graz

Rainer Peter

Co-authors 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

© Med Uni Graz • Imprint