San Antonio Cardiovascular Proteomics Center, Barshop Institute for Longevity and Aging Studies, Division of Geriatrics, Gerontology and Palliative Medicine, Department of Medicine, The University of Texas Health Science Center at San Antonio, 15355 Lambda Drive, MC 7755, San Antonio, TX 78245, USA.
J Cardiovasc Transl Res. 2012 Dec;5(6):848-57. doi: 10.1007/s12265-012-9398-z. Epub 2012 Aug 28.
The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.
细胞外基质 (ECM) 通过充当细胞的支架为组织提供结构支撑，因此 ECM 维持着正常的组织稳态，并在损伤后介导修复反应。在心肌梗死 (MI) 发生时，左心室 (LV) 的 ECM 表达通常会上调，这通过调节瘢痕形成来调节 LV 重塑。ECM 通过调节生长因子释放和细胞黏附直接影响瘢痕形成，通过调节炎症、血管生成和成纤维细胞反应间接影响瘢痕形成。这篇综述总结了目前关于 ECM 表达模式和心肌成纤维细胞机制的文献，重点讨论了 ECM 对 MI 的反应。此外，我们还讨论了未来需要研究的领域，以更好地了解 ECM 作用的分子机制，无论是一般情况下还是作为优化梗死愈合的手段。
