Cardiac Fibrosis: The Fibroblast Awakens.
Cardiac Fibrosis: The Fibroblast Awakens.
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心脏纤维化：成纤维细胞觉醒。
DOI：
10.1161/circresaha.115.306565
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发表时间：
2016-03-18
影响因子：
20.1
通讯作者：
Blaxall BC
中科院分区：
文献类型：
--
作者：
Travers JG;Kamal FA;Robbins J;Yutzey KE;Blaxall BC
心肌纤维化是一个重大的全球健康问题，几乎与所有形式的心脏病有关。心脏成纤维细胞是心脏中一种重要的细胞类型，负责细胞外基质的稳态；然而，在损伤后，这些细胞转化为肌成纤维细胞表型并促进心脏纤维化。这种重构包括心室扩张、心肌细胞肥大和细胞凋亡等病理改变，最终导致心力衰竭。尽管纤维化在心血管疾病中至关重要，但我们对这种细胞群的有限理解阻碍了有效靶向这种细胞类型及其对疾病进展的病理贡献的潜在疗法的发展。本文综述了目前关于成纤维细胞的起源和作用、已知影响心肌损伤后成纤维细胞功能的介质和信号通路，以及正在研究的减轻心脏纤维化的新治疗策略。
Myocardial fibrosis is a significant global health problem associated with nearly all forms of heart disease. Cardiac fibroblasts comprise an essential cell type in the heart that is responsible for the homeostasis of the extracellular matrix; however upon injury, these cells transform to a myofibroblast phenotype and contribute to cardiac fibrosis. This remodeling involves pathological changes that include chamber dilation, cardiomyocyte hypertrophy and apoptosis, and ultimately leads to the progression to heart failure. Despite the critical importance of fibrosis in cardiovascular disease, our limited understanding of this cell population impedes the development of potential therapies that effectively target this cell type and its pathological contribution to disease progression. This review summarizes current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis.