T-cell regulation of fibroblasts and cardiac fibrosis

被引:29
作者
Bradshaw, Amy D. [1 ]
DeLeon-Pennell, Kristine Y. [1 ]
机构
[1] Med Univ South Carolina, Ralph H Johnson Vet Affairs Med Ctr, Dept Med, Div Cardiol, 109 Bee St, Charleston, SC 29401 USA
关键词
Fibrosis; Myocardial infarction; Inflammation; T-cell; Sex; Age; MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; ESTROGEN PLUS PROGESTIN; GROWTH-FACTOR; EXTRACELLULAR-MATRIX; STROKE SENSITIVITY; MOUSE MODEL; INFARCTION; EXPRESSION; INFLAMMATION; LYMPHOCYTES;
D O I
10.1016/j.matbio.2020.04.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. 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. (c) 2020 Elsevier B.V. All rights reserved.
引用
收藏
页码:167 / 175
页数:9
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