Stanford Cardiovascular Institute, Department of Medicine, Division of Cardiology Stanford University School of Medicine, Stanford, CA 94305, U.S.A.
Department of Medicine, University of Toronto, Toronto, Canada.
Clin Sci (Lond). 2019 Nov 15;133(21):2217-2220. doi: 10.1042/CS20190866.
Cardiac fibrosis is important for wound healing, regeneration and producing the extracellular matrix (ECM) that provides the scaffold for cells. In pathological situations, fibroblasts are activated and remodel the ECM. In volume 133, issue 17 of Clinical Science, Yang et al. discovered that the miR-214-3p/NLRC5 axis is important for fibroblast-to-myofibroblast transition (FMT) and ECM remodelling in a pressure overload model of fibrosis [Clin. Sci. (2019) 133(17), 1845-1856]. This discovery helps to explain the complicated regulation of cardiac fibrosis. It also underscores the need for more investigation into the mechanisms of cardiac fibrosis to develop better diagnostic modalities and therapeutic options in heart failure.
心脏纤维化对于伤口愈合、再生和产生细胞外基质 (ECM) 以提供细胞支架很重要。在病理情况下，成纤维细胞被激活并重塑 ECM。在《临床科学》第 133 卷第 17 期上，Yang 等人发现 miR-214-3p/NLRC5 轴对于纤维化的压力超负荷模型中成纤维细胞向肌成纤维细胞转化 (FMT) 和 ECM 重塑很重要[Clin. Sci. (2019) 133(17), 1845-1856]。这一发现有助于解释心脏纤维化的复杂调控机制。它还强调了需要进一步研究心脏纤维化的机制，以开发更好的心力衰竭诊断方法和治疗选择。
