<div class="csl-bib-body">
<div class="csl-entry">Hardy, S., Liesinger, L., Patrick, R., Poettler, M., Rech, L., Gindlhuber, J., Mabotuwana, N., Ashour, D., Stangl, V., Bigland, M., Murtha, L., Starkey, M., Scherr, D., Hansbro, P. M., Hoefler, G., Ramos, G., Cochain, C., Harvey, R., Birner-Grünberger, R., … Rainer, P. P. (2023). Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction. <i>JACC: Basic to Translational Science</i>. https://doi.org/10.1016/j.jacbts.2023.05.010</div>
</div>
-
dc.identifier.issn
2452-302X
-
dc.identifier.uri
http://hdl.handle.net/20.500.12708/188039
-
dc.description.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.
en
dc.description.sponsorship
FWF Fonds zur Förderung der wissenschaftlichen Forschung (FWF)
-
dc.language.iso
en
-
dc.publisher
Elsevier
-
dc.relation.ispartof
JACC: Basic to Translational Science
-
dc.rights.uri
http://creativecommons.org/licenses/by-nc-nd/4.0/
-
dc.subject
extracellular matrix
en
dc.subject
Fibroblasts
en
dc.subject
fibrosis
en
dc.subject
heart
en
dc.subject
inflammation
en
dc.subject
myocardial infarction
en
dc.title
Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction
en
dc.type
Article
en
dc.type
Artikel
de
dc.rights.license
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
en
dc.rights.license
Creative Commons Namensnennung - Nicht kommerziell - Keine Bearbeitungen 4.0 International
de
dc.contributor.affiliation
Medical University of Graz, Austria
-
dc.contributor.affiliation
UNSW Sydney, Australia
-
dc.contributor.affiliation
Medical University of Graz, Austria
-
dc.contributor.affiliation
Medical University of Graz, Austria
-
dc.contributor.affiliation
Ludwig Boltzmann Institute for Lung Vascular Research, Austria
