The role of mitochondria in metabolic disease: a special emphasis on heart dysfunction

FEDERICO, MARILÉN; DE LA FUENTE, SERGIO; PALOMEQUE, JULIETA; SHEU, SHEY-SHING

THE JOURNAL OF PHYSIOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2021

0022-3751

Metabolic diseases (MetD) embrace a series of pathologies characterize by abnormal body glucose usage. The known diseases included in this group are metabolic syndrome, prediabetes and diabetes mellitus type 1 and 2, all of them are chronic pathologies that present metabolic disturbances and are classified as multi-organ diseases. Cardiomyopathy has been extensively described in diabetic patients without overt macrovascular complications. The heart is severely damaged during the progression of the disease, in fact, diabetic cardiomyopathies are the main cause of death in MetD. Insulin resistance, hyperglycemia, and increased free fatty acid metabolism promote cardiac damage through mitochondria. These organelles supply most of the energy that the heart needs to beat and control essential cellular functions, including Ca2+ signaling modulation, reactive oxygen species production, and apoptotic cell death regulation. Several aspects of the common mitochondrial functions have been described to be altered in diabetic cardiomyopathies include impairments of energy metabolism, compromises of mitochondrial dynamics, deficiencies in the Ca2+ handling, increases in ROS production, and a higher probability of mitochondrial permeability transition pore opening. Therefore, the mitochondrial role in MetD mediated heart dysfunction has been studied extensively to identify potential therapeutic targets for improving cardiac performance. Herein we review the cardiac pathology in metabolic syndrome, prediabetes, and diabetes mellitus, focusing on the role of mitochondrial dysfunctions.