Abstract
Epidemic of obesity accelerates the increase in the number of patients with obesity cardiomyopathy. Thioredoxin interacting protein (TXNIP) has been implicated in the pathogenesis of multiple cardiovascular diseases. However, its specific role in obesity cardiomyopathy is still not well understood. Here, we evaluated the role of TXNIP in obesity-induced cardiomyopathy by feeding wild-type and txnip gene knockout mice with either normal diet or high-fat diet (HFD) for 24 weeks. Our results suggested that TXNIP deficiency improved mitochondrial dysfunction via reversing the shift from mitochondrial fusion to fission in the context of chronic HFD feeding, thus promoting cardiac fatty acid oxidation to alleviate chronic HFD-induced lipid accumulation in the heart, and thereby ameliorating the cardiac function in obese mice. Our work provides a theoretical basis for TXNIP exerting as a potential therapeutic target for the interventions of obesity cardiomyopathy.