Meng Wei

TL;DR: In a mouse model of acute doxorubicin-induced cardiotoxicity, cardiomyocyte-specific deletion of Rac1 inhibited NADPH oxidase activation and ROS production, prevented cardiac cell death, and improved myocardial function in Rac1 knockout mice and therapeutic administration of the specific Rac1 inhibitor NSC23766 achieved similar cardio-protective effects.

TL;DR: Deletion of Capn4 reduced apoptosis, limited infarct expansion, prevented left ventricle dilation, and reduced mortality in Capn 4-ko mice, which was accompanied by down-regulation of hypertrophic genes and profibrotic genes.

TL;DR: The results of this analysis suggest that a target HbA(1c) level of 7.0-7.9% may be a better glycemic control target than that of <7.0% in patients with established type 2 diabetes mellitus.

TL;DR: Rac1 activation increases I/R injury in diabetic hearts and the role of Rac1 signaling is mediated, at least in part, through calpain activation.

TL;DR: Over-expression of calpastatin enhances doxorubicin-induced cardiac injuries through calpain inhibition and thus, calpains may protect cardiomyocytes against dox orubicIn-induced cardiotoxicity.