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Wei Y.,Shanghai JiaoTong University | Wei Y.,Shanghai Songjiang Center Hospital | Liu S.-W.,Shanghai JiaoTong University | Zhao L.-Q.,Shanghai JiaoTong University | And 3 more authors.
Medical Hypotheses | Year: 2012

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice, but its pathogenesis is incompletely understood. Current evidences have highlighted the progression of atrial fibrosis and electrophysiological remodeling in AF development. Lysophosphatidic acid (LPA), the simplest phospholipd, is associated with fibrotic disease and promotes proliferation of a wide variety of fibroblast. It was demonstrated that LPA stimulation in many cell types such as human endothelial cells, human renal fibroblasts, and myoblasts, significantly upregulates connective tissue growth factor (CTGF) expression, which acts as a downstream signaling effector for transforming growth factor-β1 (TGF-β1) to drive fibrosis. We hypothesized that LPA could also evoke growth factor-like responses to atrial fibroblast, and subsequently induce atrial fibrosis to trigger AF. LPA is also verified to involve in numerous electrophysiological activities in non-myocardiocytes. So LPA is a possible cause of AF by initiating fibrosis response and altering electrophysiological properties in atrium. If the hypothesis is confirmed, LPA will act as a new target for AF treatment and administration of LPA receptor blockers may be applied in the prophylaxis of AF. © 2012 Elsevier Ltd. Source


Wei Y.,Shanghai JiaoTong University | Wei Y.,Shanghai Songjiang Center Hospital | Zhao L.-q.,Shanghai JiaoTong University | Qi B.-z.,Shanghai JiaoTong University | And 8 more authors.
PLoS ONE | Year: 2012

Lysophosphatidic acid (LPA) has diverse actions on the cardiovascular system and is widely reported to modulate multiple ion currents in some cell types. However, little is known about its electrophysiological effects on cardiac myocytes. This study investigated whether LPA has electrophysiological effects on isolated rabbit myocardial preparations. The results indicate that LPA prolongs action potential duration at 90% repolarization (APD90) in a concentration- and frequency-dependent manner in isolated rabbit ventricular myocytes. The application of extracellular LPA significantly increases the coefficient of APD90 variability. LPA increased L-type calcium current (ICa,L) density without altering its activation or deactivation properties. In contrast, LPA has no effect on two other ventricular repolarizing currents, the transient outward potassium current (Ito) and the delayed rectifier potassium current (IK). In arterially perfused rabbit left ventricular wedge preparations, the monophasic action potential duration, QT interval, and Tpeak-end are prolonged by LPA. LPA treatment also significantly increases the incidence of ventricular tachycardia induced by S1S2 stimulation. Notably, the effects of LPA on action potentials and ICa,L are PTX-sensitive, suggesting LPA action requires a Gi-type G protein. In conclusion, LPA prolongs APD and increases electrophysiological instability in isolated rabbit myocardial preparations by increasing ICa,L in a Gi protein-dependent manner. © 2012 Wei et al. Source


Fan N.,Shanghai JiaoTong University | Zhang L.,Shanghai Songjiang Center Hospital | Xia Z.,Shanghai Songjiang Center Hospital | Peng L.,Shanghai Songjiang Center Hospital | And 2 more authors.
Journal of Diabetes Research | Year: 2016

Across-sectional study was performed in 541 type 2 diabetic patients to determine the relationship between serum uric acid (SUA) and NAFLD in type 2 diabetic patients. Clinical parameters including SUA were determined and NAFLD was diagnosed by ultrasonography. SUA was significantly higher in type 2 diabetic subjects with NAFLD than in those without NAFLD in men, but not in women. Furthermore, the prevalence rate of NAFLD increased progressively across the sex-specific SUA tertiles only in men (37.9%, 58.6%, and 72.6%, resp., P for trend < 0.001). After adjusting for confounding factors, the odd ratios (95% CI) for NAFLD were 1 (reference), 2.93 (95%CI 1.25-6.88), and 3.93 (95% CI 1.55-9.98), respectively, across the tertiles of SUA in men. Contrastingly, SUA levels in women were not independently associated with the risk of NAFLD. Our data suggests that SUA is specifically associated with NAFLD in male type 2 diabetic subjects, independent of insulin resistance and other metabolic factors. © 2016 Nengguang Fan et al. Source


Wei Y.,Shanghai JiaoTong University | Wei Y.,Shanghai Songjiang Center Hospital | Ruan L.,Huazhong University of Science and Technology | Zhou G.,Shanghai JiaoTong University | And 6 more authors.
Cardiology (Switzerland) | Year: 2012

Objectives: To investigate current evidence linking ischemic postconditioning (IPC) to cardioprotection in patients receiving primary percutaneous coronary intervention (PCI). Methods: We performed searches of PubMed, Embase, MEDLINE and Cochrane databases from January 1998 to May 2011 for identifying relevant studies comparing IPC with usual care in patients undergoing primary PCI. A meta-analysis of eligible studies was assessed by Review Manager 5.0. Results: Thirteen studies were eligible. Compared to the control, observed outcomes such as peak creatine kinase [weighted mean difference (WMD) -537.48, 95% confidence interval (CI) -779.32 to -295.65 IU/l], peak creatine kinase-myocardial band (WMD -61.11, 95% CI -76.56 to -45.66 U/l), complete ST-segment resolution (risk ratio 1.38, 95% CI 1.07 to 1.77), blush grade during reflow (WMD 0.64, 95% CI 0.49 to 0.78), corrected TIMI frame count, single-photon emission computed tomography determining infarct size, long-term left ventricular ejection fraction and short-term and long-term wall motion score indexes were improved in IPC group, with less occurrence of heart failure during the 3-month to 3.4-year follow-up. Conclusions: Though current evidence indicates that IPC provides potential cardioprotection to patients receiving primary PCI, larger adequately powered studies should be undertaken to confirm its advantages. Copyright © 2012 S. Karger AG, Basel. Source


Fan N.,Shanghai JiaoTong University | Fan N.,Shanghai Songjiang Center Hospital | Sun H.,Shanghai JiaoTong University | Wang Y.,Shanghai JiaoTong University | And 7 more authors.
PLoS ONE | Year: 2014

Obesity is associated with increased production of inflammatory mediators in adipose tissue, which contributes to chronic inflammation and insulin resistance. Midkine (MK) is a heparin-binding growth factor with potent proinflammatory activities. We aimed to test whether MK is associated with obesity and has a role in insulin resistance. It was found that MK was expressed in adipocytes and regulated by inflammatory modulators (TNF-α and rosiglitazone). In addition, a significant increase in MK levels was observed in adipose tissue of obese ob/ob mice as well as in serum of overweight/obese subjects when compared with their respective controls. In vitro studies further revealed that MK impaired insulin signaling in 3T3-L1 adipocytes, as indicated by reduced phosphorylation of Akt and IRS-1 and decreased translocation of glucose transporter 4 (GLUT4) to the plasma membrane in response to insulin stimulation. Moreover, MK activated the STAT3-suppressor of cytokine signaling 3 (SOCS3) pathway in adipocytes. Thus, MK is a novel adipocyte-secreted factor associated with obesity and inhibition of insulin signaling in adipocytes. It may provide a potential link between obesity and insulin resistance. © 2014 Fan et al. Source

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