Shen Shutong, Jiang Huimin, Bei Yihua, Xiao Junjie, Li Xinli
Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Clinical Laboratory Center, Beijing Hospital of Traditional Chinese Medicine, Beijing, China.
Cell Physiol Biochem. 2017;41(5):1830-1837. doi: 10.1159/000471913. Epub 2017 Apr 3.
Cardiac remodeling occurs after stress to the heart, manifested as pathological processes, including hypertrophy and apoptosis of cardiomyocytes, dysfunction of vascular endothelial cells and vascular smooth muscle cells as well as differentiation and proliferation of fibroblasts, ultimately resulting in progression of cardiovascular diseases. Emerging evidence has revealed that long non-coding RNAs (lncRNAs) acted as powerful and dynamic modifiers of cardiac remodeling. LncRNAs including Chaer, Chast, Mhrt, CHRF, ROR, H19, and MIAT have been implicated in cardiac hypertrophy while NRF, H19, APF, CARL, UCA, Mhrt and several other lncRNAs (n379599, n379519, n384640, n380433 and n410105) in cardiomyocyte loss and extracellular matrix remodeling. In addition, MALAT1 and TGFB2-OT1 have been reported to contribute to vascular endothelial cells dysfunction while lincRNA-p21 and lnc-Ang362 to vascular smooth muscle cells proliferation. Thus, manipulation of lncRNA expression levels through either the inhibition of disease-up-regulated lncRNAs or increasing disease-down-regulated lncRNAs represents novel therapeutic strategies for cardiac remodeling.
心脏重塑发生在心脏受到应激后，表现为病理过程，包括心肌细胞肥大和凋亡、血管内皮细胞及血管平滑肌细胞功能障碍以及成纤维细胞的分化和增殖，最终导致心血管疾病进展。新出现的证据表明，长链非编码RNA（lncRNA）是心脏重塑的强大且动态的调节因子。包括Chaer、Chast、Mhrt、CHRF、ROR、H19和MIAT在内的lncRNA与心肌肥大有关，而NRF、H19、APF、CARL、UCA、Mhrt以及其他几种lncRNA（n379599、n379519、n384640、n380433和n410105）与心肌细胞丢失和细胞外基质重塑有关。此外，据报道MALAT1和TGFB2-OT1会导致血管内皮细胞功能障碍，而lincRNA-p21和lnc-Ang362会导致血管平滑肌细胞增殖。因此，通过抑制疾病上调的lncRNA或增加疾病下调的lncRNA来操纵lncRNA表达水平，代表了心脏重塑的新治疗策略。
