- Title
- Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction
- Creator
- Hardy, Sean A.; Liesinger, Laura; 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.; Patrick, Ralph; Rainer, Peter P.; Poettler, Maria; Rech, Lavinia; Gindlhuber, Juergen; Mabotuwana, Nishani S.; Ashour, DiyaaEldin; Stangl, Verena; Bigland, Mark
- Relation
- NHMRC.1079187 http://purl.org/au-research/grants/nhmrc/1079187 & ARC DE170100226 http://purl.org/au-research/grants/arc/DE170100226
- Relation
- JACC: Basic to Translational Science Vol. 8, Issue 12, p. 1539-1554
- Publisher Link
- http://dx.doi.org/10.1016/j.jacbts.2023.05.010
- Publisher
- Elsevier
- Resource Type
- journal article
- Date
- 2023
- Description
- 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.
- Subject
- extracellular matrix; fibroblasts; fibrosis; heart; inflammation; myocardial infarction
- Identifier
- http://hdl.handle.net/1959.13/1497425
- Identifier
- uon:54347
- Identifier
- ISSN:2452-302X
- Rights
- x
- Language
- eng
- Reviewed
- Hits: 2368
- Visitors: 2313
- Downloads: 0
| Thumbnail | File | Description | Size | Format |
|---|