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Selective deletion of endothelial cell calpain in mice reduces diabetic cardiomyopathy by improving angiogenesis – published online 18/02/2019

Fig from Teng paper

Xiaomei Teng, Chen Ji, Huiting Zhong, Dong Zheng, Rui Ni, David J. Hill, Sidong Xiong, Guo-Chang Fan, Peter A. Greer, Zhenya Shen, Tianqing Peng

It is well known that cardiomyocyte dysfunction plays a central role in diabetic cardiomyopathy. However, the role of non-cardiomyocytes in this diabetic complication has not been fully addressed. In this issue, Teng et al (https://doi.org/10.1007/s00125-019-4828-y) report that endothelial cell-specific disruption of calpain reduces cardiomyopathy in a mouse model of diabetes and that the protective effect of endothelial cell-specific calpain disruption may be attributed to attenuated endothelial injury and improved angiogenesis in diabetic hearts. The authors suggest that endothelial cell calpain may promote endothelial cell death and inhibit neovascularisation via suppression of β-catenin in diabetes. They conclude that calpain-mediated endothelial cell dysfunction may be important in the pathogenesis of diabetic cardiac complications and, thus, pharmaceutical approaches targeting calpain may prove useful for the treatment of diabetes and its cardiovascular complications.

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