Artículos de revistas
Defective insulin signaling and mitochondrial dynamics in diabetic cardiomyopathy
Fecha
2015Registro en:
Biochimica et Biophysica Acta 1853 (2015) 1113–1118
DOI: 10.1016/j.bbamcr.2015.02.005
Autor
Westermeier, Francisco
Navarro Márquez, Mario F.
López Crisosto, Camila
Bravo Sagua, Roberto
Quiroga Lagos, Clara
Bustamante, Mario
Verdejo, Hugo E.
Zalaquett Sepúlveda, Ricardo
Ibacache, Mauricio
Parra Ortíz, María Valentina
Castro, Pablo F.
Rothermel, Beverly A.
Hill, Joseph A.
Lavandero González, Sergio
Institución
Resumen
Diabetic cardiomyopathy (DCM) is a common consequence of longstanding type 2 diabetes mellitus (T2DM) and
encompasses structural, morphological, functional, and metabolic abnormalities in the heart.Myocardial energy
metabolism depends on mitochondria, which must generate sufficient ATP to meet the high energy demands of
the myocardium. Dysfunctional mitochondria are involved in the pathophysiology of diabetic heart disease. A
large body of evidence implicates myocardial insulin resistance in the pathogenesis of DCM. Recent studies
showthat insulin signaling influences myocardial energy metabolismby impacting cardiomyocyte mitochondrial
dynamics and function under physiological conditions. However, comprehensive understanding of molecular
mechanisms linking insulin signaling and changes in the architecture of the mitochondrial network in diabetic
cardiomyopathy is lacking. This review summarizes our current understanding of howdefective insulin signaling
impacts cardiac function in diabetic cardiomyopathy and discusses the potential role of mitochondrial dynamics.