کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2775529 | 1152331 | 2011 | 5 صفحه PDF | دانلود رایگان |

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.
Research Highlights
► T cells affect organ fibrosis through modulating cardiac fibroblasts collagen and MMP/TIMP expression.
► Different T lymphocyte subsets play different role in inflammation-mediated cardiac fibrosis.
► Better understanding of the T cell involvement in cardiac inflammation and fibrosis facilitate the development of novel therapeutic strategies.
Journal: Experimental and Molecular Pathology - Volume 90, Issue 1, February 2011, Pages 74–78