Jian Ma

TL;DR: In this article, the authors investigated the therapeutic effects of mitochondria-targeted antioxidant mito-TEMPO on diabetic cardiomyopathy, which was administered after diabetes onset in a mouse model of streptozotocin induced type-1 diabetes and type-2 diabetic db/db mice.

TL;DR: Therapeutic silencing of miR-195 reduces myocardial hypertrophy and improves coronary blood flow and myocardials function in diabetes, at least in part by reducing oxidative damage, inhibiting apoptosis and promoting angiogenesis.

TL;DR: Myocardial hypertrophy and fibrosis in diabetic mice are attenuated by reduction of calpain function, which represents a potential novel therapeutic strategy for reversing diabetic cardiomyopathy.

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.