No abstract

diabetic cardiomyopathy (dcM) is a major cause of mortality in patients with diabetes, particularly those with type 2 diabetes. long non-coding rnas (lncrnas), including terminal differentiation-induced lncrna (Tincr), myocardial infarction-associated transcript (MiaT) and H19, serve a key role in the regulation of dcM. Micrornas (mirnas/mirs) can inhibit the expression of mrna at the post-transcriptional level, whereas lncrnas can mask the inhibitory effects of mirnas on mrna. Together, mirnas and lncrnas form a competitive endogenous non-coding rna (cerna) network that regulates the occurrence and development of various diseases. However, the regulatory role of lncrnas in dcM is unclear. in this study, a background network containing mrnas, mirnas and lncrnas was constructed using starBase and a regulatory network of dcM was screened using cytoscape. a functional lncrna, X-inactive specific transcript (XIST), was identified in the disease network and the main mirnas (mir-424-5p and mir-497-5p) that are regulated by XiST were further screened to obtain the cerna regulatory network of dcM. in conclusion, the results of this study revealed that lncrnas may serve an important role in dcM and provided novel insights into the pathogenesis of dcM.

Current therapeutic approaches have a limited effect on cardiac remodeling, which is characteristic of cardiac fibrosis and myocardial hypertrophy. In this study, we examined whether Danshenol A (DA), an active ingredient extracted from the traditional Chinese medicine Radix Salviae, can attenuate cardiac remodeling and clarified the underlying mechanisms. Using the spontaneously hypertensive rat (SHR) as a cardiac remodeling model, DA ameliorated blood pressure, cardiac injury, and myocardial collagen volume and improved cardiac function. Bioinformatics analysis revealed that DA might attenuate cardiac remodeling through modulating mitochondrial dysfunction and reactive oxygen species. DA repaired the structure/function of the mitochondria, alleviated oxidative stress in the myocardium, and restored apoptosis of cardiomyocytes induced by angiotensin II. Besides, DA inhibited mitochondrial redox signaling pathways in both the myocardium and cardiomyocytes. Thus, our study suggested that DA attenuates cardiac remodeling induced by hypertension through modulating mitochondrial dysfunction and reactive oxygen species.