期刊
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
卷 466, 期 6, 页码 1113-1127出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00424-014-1463-9
关键词
Extracellular matrix; MMP-9; Myocardial infarction; Myofibroblast; Proteomics; Review
类别
资金
- American Heart Association [14SDG18860050]
- Rapoport Foundation for Cardiovascular Research
- National Institutes of Health (NIH)/NIH Heart, Lung and Blood Institute [HHSN 268201000036C (N01-HV-00244), R01 HL075360, HL051971]
- Bio-medical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award [5I01BX000505]
- Grants-in-Aid for Scientific Research [25460662] Funding Source: KAKEN
The cardiac extracellular matrix (ECM) fills the space between cells, supports tissue organization, and transduces mechanical, chemical, and biological signals to regulate homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role in cardiac repair. A balanced turnover of ECM through regulation of synthesis by myofibroblasts and degradation by matrix metalloproteinases (MMPs) is critical for proper scar formation. In this review, we summarize the current literature on the roles of myofibroblasts, MMPs, and ECM proteins in MI-induced LV remodeling. In addition, we discuss future research directions that are needed to further elucidate the molecular mechanisms of ECM actions to optimize cardiac repair.
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