Akap1 deficiency exacerbates diabetic cardiomyopathy in mice by NDUFS1-mediated mitochondrial dysfunction and apoptosis

Conclusions/interpretationOur study provides the first evidence thatAkap1 deficiency exacerbates diabetic cardiomyopathy by impeding mitochondrial translocation of NDUFS1 to induce mitochondrial dysfunction and cardiomyocyte apoptosis. Our findings suggest thatAkap1 upregulation has therapeutic potential for myocardial injury in individuals with diabetes.
Source: Diabetologia - Category: Endocrinology Source Type: research

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Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research
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