Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 2252

Special Issue Editors


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Guest Editor
Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre CEP 90035-903, Brazil
Interests: oxidative stress

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Co-Guest Editor
Departamento de Bioquímica, Universidade Federal do Rio, Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, Bairro Santa Cecília, Porto Alegre 90035-003, RS, Brazil
Interests: oxidative stress; glial cells; neuroprotection

Special Issue Information

Dear Colleagues,

Mitochondria are the main sites of cellular oxidation and energy conversion, and most cellular ATP is produced by oxidative phosphorylation. During oxidative phosphorylation, reactive oxygen species (ROS) are produced as byproducts in mitochondria, primarily by the respiratory chain complexes I and III, and are sequestered by antioxidant defenses. Mitochondrial functionality is also maintained by the so-called mitochondrial quality control, which includes processes such as mitochondrial biogenesis, dynamics, and mitophagy. Since mitochondria are considered the main source of reactive oxygen species (ROS) production in cells, impairments in bioenergetics or any mitochondrial quality control process are often accompanied by elevated ROS and oxidative damage. Therefore, mitochondrial dysfunction and ROS production are involved in the pathophysiology of primary mitochondrial diseases, neurodegenerative disorders, cardiac insufficiency, diabetes mellitus, and aging, among others. Antioxidants and modulators of mitochondrial function can reduce mitochondrial oxidative damage and are considered promising therapeutic strategies for these pathologies. In this Special Issue, we aim to contribute to a better understanding of the pathophysiology of different pathologies characterized by mitochondrial dysfunction and reveal novel therapeutic approaches for these disorders. We look forward to your contributions to this Special Issue.

Dr. Guilhian Leipnitz
Dr. André Quincozes-Santos
Guest Editors

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Keywords

  • mitochondrial dysfunction
  • reactive oxygen species
  • bioenergetics
  • mitochondrial quality control
  • pathologies
  • protective agents

Published Papers (1 paper)

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Review

31 pages, 1047 KiB  
Review
Double Trouble: How Microbiome Dysbiosis and Mitochondrial Dysfunction Drive Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis
by Wesam Bahitham, Siraj Alghamdi, Ibrahim Omer, Ali Alsudais, Ilana Hakeem, Arwa Alghamdi, Reema Abualnaja, Faisal M. Sanai, Alexandre S. Rosado and Consolato M. Sergi
Biomedicines 2024, 12(3), 550; https://doi.org/10.3390/biomedicines12030550 - 29 Feb 2024
Viewed by 1527
Abstract
Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are closely related liver conditions that have become more prevalent globally. This review examines the intricate interplay between microbiome dysbiosis and mitochondrial dysfunction in the development of NAFLD and NASH. The combination of these [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are closely related liver conditions that have become more prevalent globally. This review examines the intricate interplay between microbiome dysbiosis and mitochondrial dysfunction in the development of NAFLD and NASH. The combination of these two factors creates a synergistic situation referred to as “double trouble”, which promotes the accumulation of lipids in the liver and the subsequent progression from simple steatosis (NAFLD) to inflammation (NASH). Microbiome dysbiosis, characterized by changes in the composition of gut microbes and increased intestinal permeability, contributes to the movement of bacterial products into the liver. It triggers metabolic disturbances and has anti-inflammatory effects. Understanding the complex relationship between microbiome dysbiosis and mitochondrial dysfunction in the development of NAFLD and NASH is crucial for advancing innovative therapeutic approaches that target these underlying mechanisms. Full article
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