Significance of mitochondria on cardiometabolic syndromes

Abstract

Metabolic syndromes (MS) are a cluster of disorders such as obesity, hypertension, dyslipidemia, and diabetes. Cardiometabolic syndrome (CMS), a branch of MS, is a group of diseases affecting cardiovascular, renal, metabolic, prothrombotic, and inflammatory abnormalities due to defects in energy metabolism. Since the emergence of molecular biology and the discovery of pathogenic mitochondrial DNA defect in the 1980s, research advances have revealed a number of common human diseases involving mitochondrial dysfunction. One of the major defects in CMS and its associated diseases is excess cellular oxidative stress and oxidative damage to mitochondrial components. In this study, we overview specific aspects of mitochondrial biology that have contributed and likely will continue enhance the progress of development of therapeutics for CMS. During the last decade, however, increasing evidence has emerged supporting the role of mitochondrial functional parameters in the genesis of various metabolism-related disorders. The biochemical pathways which modulate various mitochondrial functional indicators such as mitochondrial biogenesis, mitochondrial membrane potential, electron transport chain and ATP synthesis, intramitochondrial oxidative stress, and mitochondria- mediated cell death have been recognized in diagnosis and prognosis of various disorders associated with energy metabolism and heart function.