Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.
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
- Publisher:
- Elsevier
- Publication Type:
- Journal Article
- Citation:
- JACC Basic Transl Sci, 2023, 8, (12), pp. 1539-1554
- Issue Date:
- 2023-12
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Hardy, SA | |
dc.contributor.author | Liesinger, L | |
dc.contributor.author | Patrick, R | |
dc.contributor.author | Poettler, M | |
dc.contributor.author | Rech, L | |
dc.contributor.author | Gindlhuber, J | |
dc.contributor.author | Mabotuwana, NS | |
dc.contributor.author | Ashour, D | |
dc.contributor.author | Stangl, V | |
dc.contributor.author | Bigland, M | |
dc.contributor.author | Murtha, LA | |
dc.contributor.author | Starkey, MR | |
dc.contributor.author | Scherr, D | |
dc.contributor.author | Hansbro, PM | |
dc.contributor.author | Hoefler, G | |
dc.contributor.author | Campos Ramos, G | |
dc.contributor.author | Cochain, C | |
dc.contributor.author | Harvey, RP | |
dc.contributor.author | Birner-Gruenberger, R | |
dc.contributor.author | Boyle, AJ | |
dc.contributor.author | Rainer, PP | |
dc.date.accessioned | 2024-01-25T05:28:31Z | |
dc.date.available | 2023-05-17 | |
dc.date.available | 2024-01-25T05:28:31Z | |
dc.date.issued | 2023-12 | |
dc.identifier.citation | JACC Basic Transl Sci, 2023, 8, (12), pp. 1539-1554 | |
dc.identifier.issn | 2452-302X | |
dc.identifier.issn | 2452-302X | |
dc.identifier.uri | http://hdl.handle.net/10453/174945 | |
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. | |
dc.format | Electronic-eCollection | |
dc.language | eng | |
dc.publisher | Elsevier | |
dc.relation | http://purl.org/au-research/grants/nhmrc/GNT1079187 | |
dc.relation | http://purl.org/au-research/grants/nhmrc/1175134 | |
dc.relation | http://purl.org/au-research/grants/nhmrc/1074386 | |
dc.relation.ispartof | JACC Basic Transl Sci | |
dc.relation.isbasedon | 10.1016/j.jacbts.2023.05.010 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 1102 Cardiorespiratory Medicine and Haematology, 1103 Clinical Sciences | |
dc.subject.classification | 3201 Cardiovascular medicine and haematology | |
dc.title | Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction. | |
dc.type | Journal Article | |
utslib.citation.volume | 8 | |
utslib.location.activity | United States | |
utslib.for | 1102 Cardiorespiratory Medicine and Haematology | |
utslib.for | 1103 Clinical Sciences | |
pubs.organisational-group | University of Technology Sydney | |
pubs.organisational-group | University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | University of Technology Sydney/Strength - CFI - Centre for Inflammation | |
utslib.copyright.status | open_access | * |
dc.date.updated | 2024-01-25T05:28:25Z | |
pubs.issue | 12 | |
pubs.publication-status | Published online | |
pubs.volume | 8 | |
utslib.citation.issue | 12 |
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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