Inhibition of miR-543 alleviates cardiac fibroblast-to-myofibroblast transformation and collagen expression in insulin resistance via targeting PTEN.

Background: Myocardial interstitial fibrosis is an important manifestation of diabetic heart disease, and insulin resistance is one of the mechanisms of myocardial interstitial fibrosis. Some studies have found that miR-543 is associated with insulin resistance, but whether it plays a role in diabetic myocardial interstitial fibrosis remains unclear. This study aimed to investigate the role of miR-543 in diabetic myocardial interstitial fibrosis.

Associations of Circulating microRNA-221 and 222 With the Severity of Coronary Artery Lesions in Acute Coronary Syndrome Patients.

Circulating levels of microRNA-221 and 222 (miR-221/222) in patients with coronary artery disease (CAD) are elevated, yet the relationship between circulating miR-221/222 and the severity of coronary lesions in patients with acute coronary syndrome (ACS) remains unknown. In this study, the relative expression levels of circulating miR-221/222 in patients with ACS (n = 267) and controls (n = 71) were compared by real-time fluorescence quantitative-polymerase chain reaction (RT-qPCR). The ACS group was further divided into unstable angina pectoris (UA) group (n = 191) and acute myocardial infarction (AMI) group (n = 76).

Nitrate Esters Alleviated Coronary Atherosclerosis Through Inhibition of NF-κB-Regulated Macrophage Polarization Shift in Epicardial Adipose Tissue.

Nitrate esters have been used in clinical practice for more than one century for the treatment of angina. Their clinical effectiveness is due to vasodilator activity in arteries through a method of delivering nitric oxide or a nitric oxide-like compound. Recently, an increasing numbers of functions of this molecule in biology and pathophysiology have been discovered.

Adipocyte-Derived Exosomes Carrying Sonic Hedgehog Mediate M1 Macrophage Polarization-Induced Insulin Resistance via Ptch and PI3K Pathways.

Background/aims: Adipocyte-derived exosomes (ADEs) stimulate the activation of macrophages and contribute to the development of insulin resistance. Sonic Hedgehog (Shh) is an exosome-carrying protein and stimulates macrophages to secrete inflammatory cytokines. However, the impact of ADEs carrying Shh on the pro-inflammatory activation of macrophages and consequently, adipocyte insulin resistance is unclear.

Trimetazidine restores the positive adaptation to exercise training by mitigating statin-induced skeletal muscle injury.

Background: Exercise rehabilitation is demonstrated to improve the prognosis of patients with coronary heart disease (CHD). Statins, as the key medicine to lower cholesterol in CHD, result in skeletal muscle injury and impair exercise training adaptation. Energy metabolism dysfunction is identified as the potential mechanism underlying statin-induced skeletal muscle injury.

Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE /LDLR mouse via a PPARγ/CD36 pathway.

The aim of this study was to investigate whether overexpression of STAMP2 improves insulin resistance by regulating angiogenesis in adipose tissues. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. Samples were obtained from epididymal, subcutaneous and brown adipose tissues.

Adipose-derived stem cells were impaired in restricting CD4T cell proliferation and polarization in type 2 diabetic ApoE mouse.

Background: Atherosclerosis (AS) is the most common and serious complication of type 2 diabetes mellitus (T2DM) and is accelerated via chronic systemic inflammation rather than hyperglycemia. Adipose tissue is the major source of systemic inflammation in abnormal metabolic state. Pro-inflammatory CD4T cells play pivotal role in promoting adipose inflammation.

Testosterone delays vascular smooth muscle cell senescence and inhibits collagen synthesis via the Gas6/Axl signaling pathway.

Testosterone deficiency is associated with a higher incidence of cardiovascular diseases in men. However, its effect on cell senescence, which plays a causal role in vascular aging, remains unclear. Here, we tested the hypothesis that testosterone alleviated vascular smooth muscle cell (VSMC) senescence and collagen synthesis via growth arrest-specific protein 6 (Gas6)/Axl- and Akt/FoxO1a-dependent pathways.

Early administration of trimetazidine attenuates diabetic cardiomyopathy in rats by alleviating fibrosis, reducing apoptosis and enhancing autophagy.

Background: Trimetazidine, as an anti-ischemic and antioxidant agent, has been demonstrated to have many cardioprotective effects. However, whether early administration of trimetazidine has an effect on diabetic cardiomyopathy and the mechanisms underlying the effect have not yet been elucidated.

Methods: We established a type 2 DCM rat model by high-fat diet and low-dose streptozotocin.

Prostaglandin F2α receptor silencing attenuates vascular remodeling in rats with type 2 diabetes.

Background: Vascular remodeling is an important feature of diabetic macrovascular complications. The prostaglandin F2α receptor (FP), the expression of which is upregulated by insulin resistance and diabetes, is reportedly involved in myocardial remodeling. In this study, we aimed to investigate whether the FP receptor is implicated in diabetes-induced vascular remodeling.

Pitavastatin calcium improves endothelial function and delays the progress of atherosclerosis in patients with hypercholesterolemia.

Background: Statins have proven efficacy in inhibiting the onset and progress of atherosclerosis. The effectiveness of pitavastatin in reversing carotid atherosclerosis associated with hypercholesterolemia (HC) is unknown.

Objectives: To explore the simultaneous effects of pitavastatin calcium on brachial arterial flow-mediated vasodilatation (FMD), carotid intima-media thickness (IMT), and arterial stiffness (β), three surrogate markers of atherosclerosis were studied in HC patients.

Association between single nucleotide polymorphisms in thrombospondins genes and coronary artery disease: A meta-analysis.

Objective: This study aimed to assess the association between single nucleotide polymorphisms in thrombospondin-1 (THBS1), thrombospondin-2 (THBS2), thrombospondin-4 (THBS4) and coronary artery disease (CAD) risk.

Methods: Electronic databases were searched before June, 2014 to obtain articles associated with thrombospondin polymorphisms and CAD risk. After identifying case-control studies, odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to pool effect sizes.

Gas6 delays senescence in vascular smooth muscle cells through the PI3K/ Akt/FoxO signaling pathway.

Background/aims: Growth arrest-specific protein 6 (Gas6) is a cytokine that can be synthesized by a variety of cell types and secreted into the extracellular matrix. Previous studies have confirmed that Gas6 is involved in certain pathophysiological processes of the cardiovascular system through binding to its receptor, Axl. In the present study, we investigated the role of Gas6 in cellular senescence and explored the mechanisms underlying its activity.

MicroRNA-21, induced by high glucose, modulates macrophage apoptosis via programmed cell death 4.

MicroRNA-21 (miR-21) has been found to promote cell proliferation and survival. It has also been shown to exhibit an increased expression in a number of forms of cardiovascular disease. However, the mechanisms underlying the involvement of miR-21 in atherosclerosis remain to be elucidated.

Visceral adiposity index score indicated the severity of coronary heart disease in Chinese adults.

Background: Visceral adiposity contributes to cardiometabolic risk, and visceral adiposity index (VAI) had significant correlation with visceral adiposity. We aimed to explore whether VAI was associated with cardiac structure and function and assess the impact of the cut-off points of VAI defining visceral adipose dysfunction (VAD) on the severity of coronary heart disease (CHD).

Methods: A total of 95 patients with CHD were divided into Control (nondiabetic CHD patients) and DM group (diabetic CHD patients).

Silencing of activin receptor-like kinase 7 alleviates aortic stiffness in type 2 diabetic rats.

Aim: Arterial stiffness is an important feature of diabetic macrovascular complications. Activin receptor-like kinase 7 (ALK7), a member of type I transforming growth factor-β (TGF-β) receptors, is correlated with pathogenic risks of type 2 diabetes mellitus and cardiovascular diseases and may be involved in cardiovascular remodeling. We aimed to investigate whether ALK7 is implicated in diabetes-induced aortic stiffness.

FP-receptor gene silencing ameliorates myocardial fibrosis and protects from diabetic cardiomyopathy.

Unlabelled: Prostaglandin F2(α)-F-prostanoid (PGF2(α)-FP) receptor is closely related to insulin resistance, which plays a causal role in the pathogenesis of diabetic cardiomyopathy (DCM). We sought to reveal whether PGF2(α)-FP receptor plays an important part in modulating DCM and the mechanisms involved. We established the type 2 diabetes rat model by high-fat diet and low-dose streptozotocin (STZ) and then evaluated its characteristics by metabolite tests, Western blot analysis for FP-receptor expression, histopathologic analyses of cardiomyocyte density and fibrosis area.

Overexpression of STAMP2 suppresses atherosclerosis and stabilizes plaques in diabetic mice.

Our research aims to evaluate the function of the STAMP2 gene, an important trigger in insulin resistance (IR), and explore its role in macrophage apoptosis in diabetic atherosclerotic vulnerable plaques. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. The level of STAMP2 was measured by RT-PCR and Western blot.

Overexpressing STAMP2 improves insulin resistance in diabetic ApoE⁻/⁻/LDLR⁻/⁻ mice via macrophage polarization shift in adipose tissues.

STAMP2 is a counterregulator of inflammation and insulin resistance. The aim of this study is to investigate whether activation of STAMP2 improves insulin resistance by regulating macrophage polarization in adipose tissues. The diabetic ApoE⁻/⁻/LDLR⁻/⁻ mouse model was induced by high-fat diet and low-dose streptozotocin.

Activin receptor-like kinase 7 mediates high glucose-induced H9c2 cardiomyoblast apoptosis through activation of Smad2/3.

Cardiomyocyte apoptosis is an important pathological change of diabetic cardiomyopathy. How the elevated glucose levels cause cell apoptosis remains unknown. The aim of our study was to investigate whether activin receptor-like kinase 7 (ALK7)-Smad2/3 signaling pathway plays an important role in high glucose-induced cardiomyocyte apoptosis.

Prostaglandin F2α facilitates collagen synthesis in cardiac fibroblasts via an F-prostanoid receptor/protein kinase C/Rho kinase pathway independent of transforming growth factor β1.

Accumulation of collagen I and III in the myocardium is a prominent feature of interstitial fibrosis. Prostaglandin F(2α) (PGF(2α)) facilitates fibrosis by increasing collagen synthesis. However, the underlying mechanisms mediating the effect of PGF(2α) on collagen expression in cardiac fibroblasts are not yet fully elucidated.

An integrative view on the carotid artery alterations in metabolic syndrome.

Backgrounds: Metabolic syndrome (MetS) is a multiple risk factor paradigm widely considered in risk management. We aimed to investigate carotid artery alterations in MetS and the underlying risk factors.

Materials And Methods: A total of 400 Chinese subjects were recruited, divided into control (n = 200) and MetS (n = 200) groups.