Abstract
Type 2 diabetes mellitus is associated with a high risk of heart failure, in part because of its potential to induce impaired cardiac function even in the absence of coronary artery disease and hypertension. The pathogenesis of diabetic cardiomyopathy is not yet fully understood, although it is known that alterations in the cardiac substrate metabolism and energy play a significant role in the development and progression of this condition. Among these abnormalities, increased fatty acid storage and utilization, associated with reduced glucose oxidation and altered mitochondrial oxidative phosphorylation stand out. One of the key connections linking diabetes and the remarkably prevalence of cardiomyopathy is the renin angiotensin system (RAS) hyperactivation. RAS has been described for its crucial involvement in the generation and progression of diabetic cardiovascular complications, as its exacerbated activation supports mechanisms that lead to cardiomyocyte death and myocardial fibrosis. The importance of RAS blockage in the prevention of diabetic cardiomyopathy exhibits the fundamental role that RAS plays in the onset and development of this pathology. Angiotensin-converting enzyme inhibitors and blockers of angiotensin II actions denote the first-line therapy for primary and secondary prevention of cardiovascular disease in type 2 diabetic. Recent studies have revealed new features of RAS and, consequently, new therapeutic potential against diabetic cardiomyopathy. In this chapter, a description of the main mechanisms involved in the correlation between excessive activation of the RAS and type 2 diabetes is presented, with attention on mechanisms associated to pathogenesis and progression of diabetic cardiomyopathy.
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Gomes, K.P., Jadli, A.S., Patel, V.B. (2023). Renin Angiotensin System in the Pathophysiology of Diabetic Cardiomyopathy in Type 2 Diabetes. In: Dhalla, N.S., Bhullar, S.K., Shah, A.K. (eds) The Renin Angiotensin System in Cardiovascular Disease. Advances in Biochemistry in Health and Disease, vol 24. Springer, Cham. https://doi.org/10.1007/978-3-031-14952-8_15
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