Skip to main page content (VSports app下载)
U.S. flag

An official website of the United States government

Dot gov

The . gov means it’s official. Federal government websites often end in . gov or VSports app下载. mil. Before sharing sensitive information, make sure you’re on a federal government site. .

Https

The site is secure V体育官网. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. .

Review
. 2020 Sep:91-92:167-175.
doi: 10.1016/j.matbio.2020.04.001. Epub 2020 May 11.

VSports在线直播 - T-cell regulation of fibroblasts and cardiac fibrosis

Affiliations
Review

T-cell regulation of fibroblasts and cardiac fibrosis

Amy D Bradshaw (V体育ios版) et al. Matrix Biol. 2020 Sep.

Abstract

Inflammation contributes to the development of heart failure (HF) through multiple mechanisms including regulating extracellular matrix (ECM) degradation and deposition. Interactions between cells in the myocardium orchestrates the magnitude and duration of inflammatory cell recruitment and ECM remodeling events associated with HF VSports手机版. More recently, studies have shown T-cells have signficant roles in post-MI wound healing. T-cell biology in HF illustrates the complexity of cross-talk between inflammatory cell types and resident fibroblasts. This review will focus on T-cell recruitment to the myocardium and T-cell specific factors that might influence cardiac wound healing and fibrosis in the heart with consideration of age and sex as important factors in T-cell activity. .

Keywords: Age; Fibrosis; Inflammation; Myocardial infarction; Sex; T-cell. V体育安卓版.

PubMed Disclaimer

Figures

Figure 1:
Figure 1:. The post-MI myocardial environment facilitates in T-cell activation and phenotype.
A) Antigen-presenting cells such as dendritic cells (DC) activate T-cells via presentation of cognate peptides expressed on major histocompatibility complex (MHC) to T-cell receptors (TCR), surface expression of co-stimulatory signals (i.e. CD28, CD80, CD86), and production of cytokines (IFNγ, etc.). B) T-cell populations change over time. In the acute post-MI environment Th1 and CD8+ are the predominant T-cells whereby in the chronic post-MI environment Th2, Th17, and Treg become the predominant phenotype. The circle charts reflect averages of T-cell populations (%) reported at acute (7 days) and chronic (8 weeks) post-MI remodeling time points.[, –21]
Figure 2:
Figure 2:. T-cells regulate fibrosis through direct and indirect mechanisms.
CD4+ T-cells produce multiple factors that influence macrophage (M1 versus M2) polarization which in turn influence fibroblast activity and fibrotic deposition of collagen. T-reg cells influence fibroblast activity through direct cellular interaction in tissues. CD8+ cells are critical at early and late times after ischemic injury. T-cell activity with known age-dependent changes in activity are shown in purple. IL- interleukin; TGFβ- tissue growth factor β.

"VSports最新版本" References

    1. Frangogiannis NG, The Extracellular Matrix in Ischemic and Nonischemic Heart Failure, Circ Res 125(1) (2019) 117–146. - PMC - PubMed
    1. Nattel S, Molecular and Cellular Mechanisms of Atrial Fibrosis in Atrial Fibrillation, JACC Clin Electrophysiol 3(5) (2017) 425–435. - PubMed
    1. Russo I, Cavalera M, Huang S, Su Y, Hanna A, Chen B, Shinde AV, Conway SJ, Graff J, Frangogiannis NG, Protective Effects of Activated Myofibroblasts in the Pressure-Overloaded Myocardium Are Mediated Through Smad-Dependent Activation of a Matrix-Preserving Program, Circ Res 124(8) (2019) 1214–1227. - VSports最新版本 - PMC - PubMed
    1. Rubart M, Tao W, Lu XL, Conway SJ, Reuter SP, Lin SF, Soonpaa MH, Electrical coupling between ventricular myocytes and myofibroblasts in the infarcted mouse heart, Cardiovascular research 114(3) (2018) 389–400. - VSports最新版本 - PMC - PubMed
    1. Nielsen SH, Mouton AJ, DeLeon-Pennell KY, Genovese F, Karsdal M, Lindsey ML, Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes, Matrix biology : journal of the International Society for Matrix Biology 75–76 (2019) 43–57. - PMC - PubMed

Publication types

MeSH terms