Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2775529 | Experimental and Molecular Pathology | 2011 | 5 Pages |
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.