Abstract
Exenatide is used to treat patients with type-2 diabetes and it also exerts cardioprotective effects. Here, we tested whether Exenatide attenuates hyperglycemia-related cardiomyocyte damage by inhibiting endoplasmic reticulum (ER) stress and the NF-κB signaling pathway. Our results demonstrated that hyperglycemia activates the NF-κB signaling pathway, eliciting ER stress. We also observed cardiomyocyte contractile dysfunction, inflammation, and cell apoptosis induced by hyperglycemia. Exenatide treatment inhibited inflammation, improved cardiomyocyte contractile function, and rescued cardiomyocyte viability. Notably, re-activation of the NF-κB signaling pathway abolished Exenatide’s protective effects on hyperglycemic cardiomyocytes. Taken together, our results demonstrate that Exenatide directly reduces hyperglycemia-induced cardiomyocyte damage by inhibiting ER stress and inactivating the NF-κB signaling pathway.
Highlights
Excessive glucose intake is considered an independent risk factor for the development of obesity and diabetes
Exenatide improves cardiomyocyte viability and reduces inflammation response induced by hyperglycemia
Hyperglycemia was induced in cardiomyocytes [20], which were treated with Exenatide
Summary
Excessive glucose intake is considered an independent risk factor for the development of obesity and diabetes. The primary complications of diabetes or obesity include diabetic cardiomyopathy, neuropathy, hyperglycemia-related kidney damage, retinopathy, and food damage. Cardiovascular complications account for most of diabetes-related deaths [1]. Despite numerous efforts into advancing therapeutic approaches for diabetes, anti-diabetic medications do not seem to prevent the cardiovascular damage induced by diabetes. Exenatide, a glucagon-like protein-1 receptor agonist, was clinically used to treat patients with type-2 diabetes. While cardioprotective effects have been reported for Exenatide, the underlying molecular mechanisms remain unclear [2, 3]
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