The results showed that endothelial dysfunction and increased OS were present in subjects with IGT and IFG, indicating endothelial damage in these stages.

Edited by Tamas DalmayKeywords: miRNA Ischemic Heart disease IGF2 Angiogenesis SRF a b s t r a c t Angiogenesis, a key factor in ischemic heart disease, is rapidly initiated in response to hypoxic or ischemic conditions. MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the control of angiogenesis renders them very attractive in the development of new approaches for restoring the angiogenic balance. In the present study, we explored that miR-483-5p, a microRNA embedded in the intron of insulin-like growth factor 2 (Igf2), acts as an endogenous angiogenesis-inhibiting factor. We identified that serum response factor (SRF) is one of miR-483-5p target genes. These findings indicated that the miR-483-5p-SRF pathway may offer a novel strategy for treatment with angiogenesis in ischemic heart disease patients.

Significant down-regulation of miR-34a in hypoxic lung tissue, pulmonary artery and PASMCs was identified and then effects of miR-34a in modulating cell proliferation in human pulmonary artery smooth muscle cells (hPASMCs) was investigated in vitro. Reduction of miR-34a levels in hPASMCs caused increased proliferation and these effects were reversed by overexpression of miR-34a. miR-34a overexpression down-regulated platelet-derived growth factor receptor alpha (PDGFRA) expression, which is a key factor in PAH development. These results suggest that miR-34a is a potential regulator of proliferation in PASMCs, and that it could be used as a novel treatment strategy in PAH.

Myocardial ischemia and reperfusion (MI/R) is associated with an intense inflammatory reaction, which may lead to myocyte injury. In this study, we investigated the effect of quercetin, an inhibitor of c-Jun N-terminal kinase on ischemia/reperfusion injury in isolated rat hearts. Rat models of MI/R were induced by coronary occlusion followed by reperfusion, treatment of rats with quercetin (1.0 mg/kg, i.v.) induced a significant reduction of infarct volume and improvements in baseline hemodynamic abnormalities (P< 0.05). Quercetin treatment also attenuated the expression of both TNF-alpha (TNF-α) and interleukin-10 (IL-10) and lowered the serum levels of inflammatory cytokine (P < 0.05). These findings suggested that quercetin treatment significantly attenuated MI/R injury primarily through anti-inflammatory effects.

Chronic continuous hippocampal DBS demonstrated a potential efficiency and safety in nonlesional refractory mesial temporal lobe epilepsy and might represent an effective therapeutic option for these patients.