Yunping Chen

TL;DR: A novel mechanism of allicin attenuating cardiac hypertrophy is revealed whichallicin could inhibit excessive autophagy via activating PI3K/Akt/mTOR and MAPK/ERK/m TOR signaling pathways.

TL;DR: The results revealed that CAR administration significantly protected the heart function, attenuated myocardial infarct size, increased SOD and CAT levels, reduced MDA level and especially decreased cardiomyocytes apoptosis, and the cardioprotective effects of CAR may be attributed to its antioxidant and antiapoptotic activities through activations of the MAPK/ERK and Akt/eNOS signaling pathways.

TL;DR: The AMPK activation improved the impaired cardiac function of cardiac fibrosis rats and decreased interstitial fibrosis and activated the miR-29 family upregulation, which prevented the development of heart fibrosis.

TL;DR: This study uncovered and systematically characterized global properties of mRNA-related ceRNA cross-talks across CVDs, which may provide a new layer for exploring biological mechanisms and shed new light on cardiology.

TL;DR: Interestingly, it was found that activated TRPV3 in Ang II–induced cardiomyocyte hypertrophy was accompanied with increasing intracellular calcium concentration, promoting calcineurin, and phosphorylated CaMKII protein expression, and enhancing NFATc3 nuclear translocation, revealing that TRPv3 might be a potential therapeutic target for cardiachypertrophy.