Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8473938 | Journal of Molecular and Cellular Cardiology | 2016 | 5 Pages |
Abstract
Lymphocytes came recently into focus as modulators of non-infectious myocardial diseases. Several lines of experimental evidence now indicate that CD4+ T-cells can influence the healing and scarring processes that follow a myocardial infarction episode. Furthermore, such heart-directed T-cell activity has also been implicated in the pathogenesis cardiac remodeling that develops in response to chronic pressure-overload conditions. Mechanistically, different T-cell subsets can secrete several mediators and growth factors that influence the myocardial molecular milieu and directly interfere with the macrophages' and fibroblasts' activity. Therefore, the present review summarizes the current experimental evidence on the role of T-cells in myocardial scar formation after infarction and myocardial fibrosis as central mechanism of ventricular remodeling.
Keywords
FOXP3TGF-βTNFIL-13IL-5NOS2TregIL-17IFN-γIL-10IL-4Myocardial infarctioninterferon-gammainterleukin-4Interleukin-5Interleukin-10Interleukin-13interleukin-17transforming growth factor-betaTeffforkhead box P3T-helper cellRegulatory T-cellT-cellsinducible nitric oxide synthaseHealingtumor necrosis factorMyocardial fibrosis
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Authors
Gustavo Ramos, Ulrich Hofmann, Stefan Frantz,