Key result
Resistin plays a central role in the maladaptive cardiac phenotype seen in diabetic hearts, suggesting that targeting its levels may be a viable therapeutic strategy for diabetic cardiomyopathy.
Why the study?
Does targeting resistin levels improve outcomes in patients with diabetic cardiomyopathy?
Does targeting resistin levels improve outcomes in patients with diabetic cardiomyopathy?
Answers are grounded in this paper and cite their sources.
This editorial highlights the potential of targeting the adipokine resistin as a therapeutic strategy for managing diabetic cardiomyopathy and preventing heart failure in diabetic patients.
Cardiovascular disease, including heart failure (HF), is the major cause of death in patients with diabetes. A contributing factor to the occurrence of HF in such patients is the development of diabetic cardiomyopathy. Recent evidence demonstrates that perturbations associated with adipokines secretion and signaling result in lusitropic and inotropic defects in diabetic cardiomyopathy. This perspective editorial will discuss the central role of resistin, a recently discovered adipokine, in the maladaptive cardiac phenotype seen in diabetic hearts. Given the pleiotropic effects of resistin, strategies targeting the control of resistin levels may constitute a potentially viable therapeutic utility in patients with diabetes and diabetes-induced cardiovascular diseases.
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Djamel Lebeche (2015) conducted an editorial in Diabetic cardiomyopathy. Resistin was evaluated. Resistin plays a central role in the maladaptive cardiac phenotype seen in diabetic hearts, suggesting that targeting its levels may be a viable therapeutic strategy for diabetic cardiomyopathy.
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