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细胞外基质蛋白-1作为心肌梗死后炎症诱导纤维化的介质

Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.

作者信息

Hardy Sean A, Liesinger Laura, Patrick Ralph, Poettler Maria, Rech Lavinia, Gindlhuber Juergen, Mabotuwana Nishani S, Ashour DiyaaEldin, Stangl Verena, Bigland Mark, 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, Rainer Peter P

机构信息

Department of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.

School of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.

出版信息

JACC Basic Transl Sci. 2023 Aug 16;8(12):1539-1554. doi: 10.1016/j.jacbts.2023.05.010. eCollection 2023 Dec.

DOI:10.1016/j.jacbts.2023.05.010
PMID:38205347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10774582/
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.

摘要

不可逆性纤维化是心肌梗死（MI）和心力衰竭的一个标志。细胞外基质蛋白-1（ECM-1）在这些心脏中上调，定位于纤维化、炎症和血管周围区域。ECM-1主要来源于未受伤的人类和小鼠心脏中的成纤维细胞、巨噬细胞和周细胞/血管细胞，以及心肌梗死后的M1和M2巨噬细胞和成肌纤维细胞。ECM-1刺激成纤维细胞向肌成纤维细胞转变，上调关键的纤维化和炎症途径，并抑制心脏成纤维细胞迁移。ECM-1与HuCFb细胞表面受体LRP1结合，抑制LRP1可阻止ECM-1刺激成纤维细胞向肌成纤维细胞转变，证实了一种新的ECM-1-LRP1纤维化信号轴。ECM-1可能代表了一种促进炎症-纤维化相互作用的新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/b8599ad2746d/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/af6bf598a33c/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/ad99a365337d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/189cf1b5f486/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/96be3e41dded/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/6e2f11c9727f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/b8599ad2746d/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/af6bf598a33c/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/ad99a365337d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/189cf1b5f486/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/96be3e41dded/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/6e2f11c9727f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b97b/10774582/b8599ad2746d/gr5.jpg

相似文献

[1]
Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.

JACC Basic Transl Sci. 2023-8-16

[2]
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[3]
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[4]
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[5]
CTRP3 attenuates post-infarct cardiac fibrosis by targeting Smad3 activation and inhibiting myofibroblast differentiation.

J Mol Med (Berl). 2015-12

[6]
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[7]
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[8]
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Cell Tissue Res. 2016-9

[9]
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FASEB J. 2022-2

[10]
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Eur J Cell Biol. 2023-6

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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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本文引用的文献

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