Inhibition of protein kinase C βII isoform ameliorates methylglyoxal advanced glycation endproduct-induced cardiomyocyte contractile dysfunction.

@article{Zhang2014InhibitionOP,
  title={Inhibition of protein kinase C βII isoform ameliorates methylglyoxal advanced glycation endproduct-induced cardiomyocyte contractile dysfunction.},
  author={Liwei Zhang and Dangsheng Huang and Dong Shen and Chunhong Zhang and Yongjiang Ma and Sara A. Babcock and Bingyang Chen and Jun Ren},
  journal={Life sciences},
  year={2014},
  volume={94 1},
  pages={83-91}
}
AIMS Accumulation of advanced glycation endproduct (AGE) contributes to diabetic complication including diabetic cardiomyopathy although the precise underlying mechanism still remains elusive. Recent evidence depicted a pivotal role of protein kinase C (PKC) in diabetic complications. To this end, this study was designed to examine if PKCβII contributes to AGE-induced cardiomyocyte contractile and intracellular Ca(2+) aberrations. MAIN METHODS Adult rat cardiomyocytes were incubated with… CONTINUE READING