Mineralocorticoid Receptor and Leptin: A Dangerous Liaison in the Obese Heart

Multiple factors have been proposed as being responsible for cardiac damage in the context of obesity, including aldosterone/mineralocorticoid receptor and leptin. Aldosterone exerts proinflammatory, prooxidant and profibrotic actions, which can play a key role in the development of cardiac damage associated with different pathologies, through binding of mineralocorticoid receptor (MR). Moreover, its pharmacological blockade has demonstrated to improve these situations. Different studies have demonstrated that aldosterone is inappropriately elevated in obesity and MR antagonism improves left ventricle function and reduces circulating procollagen levels in patients with obesity without other comorbidities. Leptin is locally produced in the myocardium and its production is up-regulated in obesity. This adipokine is a proinflammatory, prooxidant and profibrotic factor that can participate in the cardiac damage associated with obesity. Interactions among leptin and aldosterone have previously been reported in different scenarios and at different levels, supporting a link between leptin and MR and that could result in the potentiation of the cardiac damage associated with obesity. Therefore, the aim of this review is to discuss whether MR activation can mediate the deleterious effects of leptin in the heart in the context of obesity, as well as the potential mechanisms involved in this process.

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