Mitochondrial Oxidative Stress in Aging and Disease

Dear Colleagues,

Mitochondria are the body’s main metabolic hubs, since they house cellular respiration and other crucial processes such as biomolecules synthesis, apoptosis, and calcium regulation. Mitochondria are also involved in signaling pathways entailed in health and disease conditions through changes in metabolites concentrations and in enzyme activities. Mitochondrial respiration is a major source of reactive oxygen species (ROS), which can act both as signaling and damaging molecules. Mitochondrial oxidative stress, resulting from the prevalence of oxidants above antioxidants, is present in physiological processes, such as aging, and in pathological ones, where it can lead to neurotoxicity, genomic instability, pro-inflammatory gene transcription and cytokine release. Mitochondrial oxidative stress is always associated with dysfunction of the organelle, driving to a decreased ATP production and to several different responses that may impinge also out of mitochondria and synergistically cooperate with other pathways to the onset of overt pathologies.  Mitochondria are nowadays emerging as central players in neurodegeneration, age-related and metabolic diseases because alterations in their elaborate maintenance pathways, including also redox regulation, have increasingly been assessed as relevant in different diseases. Therefore, the ongoing trials of several kinds of antioxidants in various experimental and clinical settings aim to preserve mitochondrial redox homeostasis to maintain good health and provide a feasible therapeutical approach.

This Special Issue’s goal is to provide a broad and updated overview of the involvement of “Mitochondrial oxidative stress in aging and disease” that might shed light on model systems, patho-physiological mechanisms and novel therapeutic approaches through contributions by experts of the field in the form of research papers and critical reviews.

Prof. Dr. Vito Pesce
Dr. Angela Maria Serena Lezza
Guest Editors

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