The Antioxidant Effect of Melatonin on Mitochondrial Network

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 5290

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Department of Biomolecular Sciences, University of Urbino Carlo Bo, 61029 Urbino, Italy
Interests: apoptosis; autophagy; oxidative stress; endopasmic reticulum stress; mitochondria
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Special Issue Information

Mounting evidence from current studies has indicated that oxidative stress contributes to the development of several diseases. Mitochondria are dynamic organelles that are involved in the regulation of various cellular functions, including energy production, ROS generation, and cell death. Recent papers have highlighted that mitochondria are remodeled by fission and fusion, which are a very important metabolic demand. Mitochondrial ROS can affect fission and fusion both under physiological and stress conditions. The ROS produced by the respiratory chain inside mitochondria could be involved in fission. This phenomenon, called mitoptosis, helps to maintain the mitochondrial morphology and function, eliminating ROS-producing mitochondria. There are many molecules that potentially work as free radical scavengers; however, melatonin has an advantageous position that other antioxidants do not have. In fact, melatonin directly or indirectly limits oxidative stress. Moreover, the protective effects of melatonin on mitochondria depend on its accumulation in these organelles. Several papers have documented that melatonin has positive effects on mitochondrial dynamics. However, the underlying mechanism through which melatonin regulates the mitochondrial network is still to be investigated. The aim of this Special Issue is to collocate original research in order to spread new knowledge to a broader audience of this journal.

Prof. Francesca Luchetti
Guest Editor

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Keywords

  • • Melatonin • mitochondrial network • oxidative stress • apoptosis

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Published Papers (1 paper)

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Research

22 pages, 6746 KiB  
Article
Melatonin/Nrf2/NLRP3 Connection in Mouse Heart Mitochondria during Aging
by Marisol Fernández-Ortiz, Ramy K. A. Sayed, José Fernández-Martínez, Antonia Cionfrini, Paula Aranda-Martínez, Germaine Escames, Tomás de Haro and Darío Acuña-Castroviejo
Antioxidants 2020, 9(12), 1187; https://doi.org/10.3390/antiox9121187 - 27 Nov 2020
Cited by 40 | Viewed by 4891
Abstract
Aging is a major risk for cardiovascular diseases (CVD). Age-related disorders include oxidative stress, mitochondria dysfunction, and exacerbation of the NF-κB/NLRP3 innate immune response pathways. Some of the molecular mechanisms underlying these processes, however, remain unclear. This study tested the hypothesis that NLRP3 [...] Read more.
Aging is a major risk for cardiovascular diseases (CVD). Age-related disorders include oxidative stress, mitochondria dysfunction, and exacerbation of the NF-κB/NLRP3 innate immune response pathways. Some of the molecular mechanisms underlying these processes, however, remain unclear. This study tested the hypothesis that NLRP3 inflammasome plays a role in cardiac aging and melatonin is able to counteract its effects. With the aim of investigating the impact of NLRP3 inflammasome and the actions and target of melatonin in aged myocardium, we analyzed the expression of proteins implied in mitochondria dynamics, autophagy, apoptosis, Nrf2-dependent antioxidant response and mitochondria ultrastructure in heart of wild-type and NLRP3-knockout mice of 3, 12, and 24 months-old, with and without melatonin treatment. Our results showed that the absence of NLRP3 prevented age-related mitochondrial dynamic alterations in cardiac muscle with minimal effects in cardiac autophagy during aging. The deficiency of the inflammasome affected Bax/Bcl2 ratio, but not p53 or caspase 9. The Nrf2-antioxidant pathway was also unaffected by the absence of NLRP3. Furthermore, NLRP3-deficiency prevented the drop in autophagy and mice showed less mitochondrial damage than wild-type animals. Interestingly, melatonin treatment recovered mitochondrial dynamics altered by aging and had few effects on cardiac autophagy. Melatonin supplementation also had an anti-apoptotic action in addition to restoring Nrf2-antioxidant capacity and improving mitochondria ultrastructure altered by aging. Full article
(This article belongs to the Special Issue The Antioxidant Effect of Melatonin on Mitochondrial Network)
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