We previously established a rat model of diabetic cardiomyopathy (DCM) and found that the expression of long non-coding RNA myocardial infarction–associated transcript (MIAT) was significantly upregulated. The present study was aimed to determine the pathologic role of MIAT in the development of DCM. MIAT knockdown was found to reduce cardiomyocyte apoptosis and improve left ventricular function in diabetic rats. High glucose could increase MIAT expression and induce apoptosis in cultured neonatal cardiomyocytes. The results of luciferase reporter assay and RNA immunoprecipitation assay revealed that MIAT was targeted by miR-22-3p in an AGO2-dependent manner. In addition, the 3′-untranslated region of DAPK2 was fused to the luciferase coding region and transfected into HEK293 cells with miR-22-3p mimic, and the results showed that DAPK2 was a direct target of miR-22-3p. Our findings also indicated that MIAT overexpression could counteract the inhibitory effect of miR-22-3p on DAPK2. Moreover, MIAT knockdown was found to reduce DAPK2 expression and inhibit apoptosis in cardiomyocytes exposed to high glucose. In conclusion, our study demonstrates that MIAT may function as a competing endogenous RNA to upregulate DAPK2 expression by sponging miR-22-3p, which consequently leads to cardiomyocyte apoptosis involved in the pathogenesis of DCM.

Although visceral obesity is recognized as a risk factor for cardiovascular diseases (CVDs), the efficacy of omental fat removal in CVD treatment is still controversial. There is a need to identify other visceral fat depots for CVD management. This review aims to provide a summary on perirenal fat as an important risk factor for CVD. Studies on epidemiology, anatomy, and function of perirenal fat were reviewed. Observational studies in humans suggest that excessive perirenal fat increases the risk of hypertension and coronary heart disease. Anatomy studies prove that perirenal fat is unique compared to other connective tissues in that it is well vascularized, innervated, and drains into the lymphatic system. Other special morphological features include a complete fascia border, sympathetic-independent development of architecture, and proximity to the kidneys. Based on these anatomical features, perirenal fat regulates the cardiovascular system presumably via neural reflex, adipokine secretion, and fat–kidney interaction. These new insights suggest that perirenal fat may constitute a promising target for CVD management.

Valve interstitial cells (VICs) are responsible for maintaining the structural integrity and dynamic behaviour of the valve. Telocytes (TCs), a peculiar type of interstitial cells, have been recently identified by Popescu*s group in epicardium, myocardium and endocardium (visit http://www.telocytes.com). The presence of TCs has been identified in atria, ventricles and many other tissues and organ, but not yet in heart valves. We used transmission electron microscopy and immunofluorescence methods (double labelling for CD34 and c-kit, or vimentin, or PDGF Receptor-β) to provide evidence for the existence of TCs in human heart valves, including mitral valve, tricuspid valve and aortic valve. TCs are found in both apex and base of heart valves, with a similar density of 27–28 cells/mm2 in mitral valve, tricuspid valve and aortic valve. Since TCs are known for the participation in regeneration or repair biological processes, it remains to be determined how TCs contributes to the valve attempts to re-establish normal structure and function following injury, especially a complex junction was found between TCs and a putative stem (progenitor) cell.