Abstract

Mitochondrial dysfunction has been defined as a reduced efficiency of mitochondria to produce ATP given by a loss of mitochondrial membrane potential, alterations in the electron transport chain (ETC) function, with in-crease in reactive oxygen species (ROS) generation and decrease in oxygen consumption. During the last decades, mitochondrial dysfunction has been the focus of many researchers as a convergent point for the pathophysiology of several diseases. Numerous investigations have demonstrated that mitochondrial dysfunction is detrimental to