Abstract
Heart failure is a common and clinically significant cardiac condition that causes significant morbidity and mortality in the United States. Diabetes and hypertension are 2 of the most common comorbidities associated with heart failure. Other risk factors for heart failure include smoking, obesity, and intrinsic cardiac diseases such as myocardial infarction and valvular pathologies. All of these conditions, to some extent, cause remodeling within the cardiomyocyte, which eventually leads to the development of congestive heart failure. Over the years, using diuretics and medications that inhibit the Renin-Angiotensin-Aldosterone System has been the traditional treatment for congestive heart failure. But in recent years studies in the diabetic population revealed that sodium-glucose cotransporter-2 inhibitors had a negative impact on the remodeling of cardiomyocytes. In this review, we discuss the numerous molecular mechanisms by which these recently developed medicines inhibit remodeling in cardiomyocytes, independent of their intended effect of decreasing blood glucose levels. Furthermore, it emphasizes the use of these drugs in diabetic as well as non-diabetic patients as a promising adjunct to ongoing heart failure treatment.
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