Role of Mitochondria and ROS in Health and Disease

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: 15 November 2024 | Viewed by 69

Special Issue Editors


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Guest Editor
Department of Biology, University Federico II of Naples, Via Cinthia 26, 80126 Naples, Italy
Interests: oxidative stress; hyperthyroidism; mitochondria; vitamin E; ROS; antioxidant; insulin resistance

Special Issue Information

Dear Colleagues,

Mitochondria are complex organelles that perform multiple functions in eukaryotic cells and interact and communicate with all cellular organelles, including endoplasmic reticulum, lysosomes, cytoskeleton, peroxisomes, and the nucleus. Their principal role is to serve as a primary site for energy production in a process accompanied by the formation of potentially harmful substances, such as radicals and other reactive oxygen species (ROS), which can damage, among others, the same mitochondria that produce them. Mitochondria possess an efficient antioxidant system to counteract the harmful effects of ROS, which also makes them capable of eliminating ROS produced by other cellular sources, acting as a hub for regulating cellular ROS content.

Under basal conditions, a low ROS production is critical since ROS function as messenger molecules in various physiological processes, including adaptation to hypoxia, the regulation of autophagy, immunity, differentiation, longevity, and adaptation to exercise. Indeed, ROS are necessary to improve mitochondrial health and activate their proliferation during physical activity.

In some circumstances, including mitochondrial DNA mutations, infections, ageing, and a lack of physical activity, ROS production can increase, thus activating a vicious cycle that leads to mitochondrial dysfunction. Indeed, when mitochondrial ROS production increases, damage to components of the respiratory chain and enzymes of the Krebs cycle occurs, inducing a positive feedback loop that intensifies ROS production, resulting in damage to various cellular structures. The accumulation of oxidative damage to cellular structures and the impairment of mitochondrial wellbeing both contribute to the development of many non-communicable diseases, including age-related macular disease (AMD), neurological disorders, and metabolic diseases. This observation highlights the urgent need for a comprehensive understanding of the pathways involving ROS, with a particular focus on identifying key targets for effective therapeutic interventions.

Dr. Paola Venditti
Dr. Gaetana Napolitano
Dr. Gianluca Fasciolo
Guest Editors

Manuscript Submission Information

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Keywords

  • ROS
  • mitochondria
  • antioxidant
  • oxidative stress
  • neurological diseases
  • metabolic diseases
  • retinal diseases
  • mitochondrial disfunctions
  • mitochondria endoplasmic reticulum communication
  • mitochondrial bioenergetics
  • ageing
  • physical activity

Published Papers

This special issue is now open for submission.
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