Cardiac Fibroblast Activation Post-Myocardial Infarction: Current Knowledge Gaps

被引:150
|
作者
Ma, Yonggang [1 ]
Iyer, Rugmani Padmanabhan [1 ]
Jung, Mira [1 ]
Czubryt, Michael P. [2 ]
Lindsey, Merry L. [1 ,3 ]
机构
[1] Univ Mississippi, Med Ctr, Dept Biophys & Physiol, Mississippi Ctr Heart Res, Jackson, MS 39216 USA
[2] Univ Manitoba, Dept Physiol & Pathophysiol, Albrechtsen Res Ctr, Inst Cardiovasc Sci,St Boniface Hosp, Winnipeg, MB, Canada
[3] GV Sonny Montgomery Vet Affairs Med Ctr, Res Serv, Jackson, MS 39216 USA
基金
美国国家卫生研究院; 加拿大健康研究院;
关键词
NECROSIS-FACTOR-ALPHA; MYOCARDIAL-INFARCTION; EXTRACELLULAR-MATRIX; CHEMOATTRACTANT PROTEIN-1; SCAR FORMATION; MYOFIBROBLASTS; EXPRESSION; CELLS; FIBROSIS; GROWTH;
D O I
10.1016/j.tips.2017.03.001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
In response to myocardial infarction (MI), the wound healing response of the left ventricle (LV) comprises overlapping inflammatory, proliferative, and maturation phases, and the cardiac fibroblast is a key cell type involved in each phase. It has recently been appreciated that, early post-MI, fibroblasts transform to a proinflammatory phenotype and secrete cytokines and chemokines as well as matrix metalloproteinases (MMPs). Later post-MI, fibroblasts are activated to anti-inflammatory and proreparative phenotypes and generate anti-inflammatory and proangiogenic factors and extracellular matrix (ECM) components that form the infarct scar. Additional studies are needed to systematically examine how fibroblast activation shifts over the timeframe of the MI response and how modulation at different activation stages could alter wound healing and LV remodeling in distinct ways. This review summarizes current fibroblast knowledge as the foundation for a discussion of existing knowledge gaps.
引用
收藏
页码:448 / 458
页数:11
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