期刊
CIRCULATION RESEARCH
卷 127, 期 3, 页码 427-447出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.120.316958
关键词
fibrosis; heart failure; metabolism; mitochondria; myofibroblast
资金
- National Institutes of Health [F32HL145914, R01HL123966, R01HL136954, R01HL142271, P01HL134608]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [F30HL152564] Funding Source: NIH RePORTER
Cardiac fibrosis is mediated by the activation of resident cardiac fibroblasts, which differentiate into myofibroblasts in response to injury or stress. Although myofibroblast formation is a physiological response to acute injury, such as myocardial infarction, myofibroblast persistence, as occurs in heart failure, contributes to maladaptive remodeling and progressive functional decline. Although traditional pathways of activation, such as TGF beta (transforming growth factor beta) and AngII (angiotensin II), have been well characterized, less understood are the alterations in mitochondrial function and cellular metabolism that are necessary to initiate and sustain myofibroblast formation and function. In this review, we highlight recent reports detailing the mitochondrial and metabolic mechanisms that contribute to myofibroblast differentiation, persistence, and function with the hope of identifying novel therapeutic targets to treat, and potentially reverse, tissue organ fibrosis.
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