Department of Cardiology, First Affiliated Hospital of Harbin Medical University, 150001, China.
Exp Mol Pathol. 2011 Feb;90(1):74-8. doi: 10.1016/j.yexmp.2010.10.004. Epub 2010 Oct 19.
Cardiac fibrosis is defined as a progressive accumulation of fibrillar extracellular matrix (ECM) in the myocardium. The regulation of extracellular matrix remodeling is primarily mediated by cardiac fibroblasts (CF). Evidences suggest that various T lymphocyte phenotypes differentially affect organ fibrosis through modulating CF collagen and MMP/TIMP gene expression, MMP activity and cardiac collagen cross-linking, leading to altered ECM composition. In regard to the importance of cytokines in cardiac fibrosis and heart failure, in this review, we will address the role of different T cell subsets in inflammation-mediated cardiac fibrosis, from a distinct perspective of T cell and fibroblast interaction. We conclude that in addition to preventive strategies, therapies based on deviation of Th1/Th2 paradigm, and manipulation of Tregs and Th17 would show promising results in future studies.
心肌纤维化被定义为心肌中纤维细胞外基质（ECM）的进行性积累。细胞外基质重塑的调节主要由心脏成纤维细胞（CF）介导。有证据表明，各种 T 淋巴细胞表型通过调节 CF 胶原和 MMP/TIMP 基因表达、MMP 活性和心脏胶原交联，从而改变 ECM 组成，从而对器官纤维化产生不同的影响。关于细胞因子在心肌纤维化和心力衰竭中的重要性，在这篇综述中，我们将从 T 细胞与成纤维细胞相互作用的独特角度，探讨不同 T 细胞亚群在炎症介导的心肌纤维化中的作用。我们得出结论，除了预防策略外，基于 Th1/Th2 范式偏离和调节 Treg 和 Th17 的治疗方法在未来的研究中将会显示出有希望的结果。
