Objective To explore the molecular mechanism of Smurf2's effect on hyperglycemia-induced mesangial cell proliferation and fibrosis by targeting EYA2. Methods Mouse mesangial cells (GMCs) were cultured, and sh-Smurf2 and sh-NC vectors were transfected into GMCs induced by high glucose. Cell proliferation in blank control group (NG), high glucose treatment group (HG), high glucose + sh-NC group (HG + sh-NC), and high glucose + sh-Smurf2 group (HG + sh-Smurf2) were detected by CCK-8 and EdU. The expressions of Fibronectin, Collagen I and α-SMA proteins were detected by Western blot. CO-IP assay was employed to detect the targeting interaction between Smurf2 and EYA2, and then sh-EYA2 and sh-NC vectors were used to transfect GMCs for backtracking experiments. Results Compared with NG group, cell proliferation and protein expression of Fibronectin, Collagen I and α-SMA in HG group were significantly increased. Compared with HG group, interference with Smurf2 inhibited cell proliferation and the expression of Fibronectin, Collagen I and α-SMA proteins. CO-IP results showed a targeted interaction between Smurf2 and EYA2. Compared with HG + sh-Smurf2 group, interference with EYA2 promoted cell proliferation and the expression of Fibronectin, Collagen I and α-SMA proteins. Conclusion Interference with Smurf2 can inhibit hyperproliferation and fibrosis of GMCs induced by high glucose by upregulating EYA2.

Objective To investigate the effect of exhaustive exercise on sodium channel currents (I_Na), ECG and echocardiography parameters in a rat swimming model. Methods Rats of the exercise group were forced to swim until exhaustion each time for 9 days with 5% body weight (workload) attached to the head. A swimming session will be held at 9 am from day 1 to day 9. The criteria of exhausting exercise included the rotatingmotion in water, the significant decrease in motor coordination, and more than 10 seconds from water submerged the nose to the body resurfaced. After 1 day of recovery period, we performed ventricular myocytes isolation and used whole cell patch-clamp technique to investigate sodium channel currents, sedentary rats served as controls. In addition, echocardiography and ECG parameters were analyzed. Results After 9 days of swimming exercise, a decrease in EF and FS% was observed, however, no significant differences were found between sedentary and exercise group. In addition, no significant differences were found in heart rate, LVPWs, LVPWd, IVSs, IVSd, LVIDs, LVIDd, EDV, LV Mass between sedentary and exercise group. The following ECGs parameters were increased: P wave amplitude, P wave duration, QRS amplitude and R wave amplitude, while the other parameters remained unchanged. When compared to sedentary, peak I_Na density was enhanced by exhaustive exercise, however, exhaustive exercise didn't change the steady-state activation and inactivation of I_Na. Conclusion The P, QRS and R-wave amplitudes increased after exhaustive exercise indicating impaired myocardial depolarization, which may be caused by the enhanced I_Na. These changes could shorten the action potential, and thus may contribute to proarrhythmia in cardiomyocytes.