Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the Diseases

A decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate immune signaling cascades to intensify the infl...

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Main Authors: Simone Patergnani, Esmaa Bouhamida, Sara Leo, Paolo Pinton, Alessandro Rimessi
Format: Article
Language:English
Published: MDPI AG 2021-02-01
Series:Biomedicines
Subjects:
Online Access:https://www.mdpi.com/2227-9059/9/2/216
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author Simone Patergnani
Esmaa Bouhamida
Sara Leo
Paolo Pinton
Alessandro Rimessi
author_facet Simone Patergnani
Esmaa Bouhamida
Sara Leo
Paolo Pinton
Alessandro Rimessi
author_sort Simone Patergnani
collection DOAJ
description A decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate immune signaling cascades to intensify the inflammatory response at front of different stimuli. Here, we review the evidence that an exacerbation in the levels of mitochondrial-derived reactive oxygen species (ROS) contribute to mito-inflammation, a new concept that identifies the compartmentalization of the inflammatory process, in which the mitochondrion acts as central regulator, checkpoint, and arbitrator. In particular, we discuss how ROS contribute to specific aspects of mito-inflammation in different inflammatory-related diseases, such as neurodegenerative disorders, cancer, pulmonary diseases, diabetes, and cardiovascular diseases. Taken together, these observations indicate that mitochondrial ROS influence and regulate a number of key aspects of mito-inflammation and that strategies directed to reduce or neutralize mitochondrial ROS levels might have broad beneficial effects on inflammatory-related diseases.
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spelling doaj.art-7dacfa8935aa4007a34a9fbb1e50910a2023-12-11T17:44:22ZengMDPI AGBiomedicines2227-90592021-02-019221610.3390/biomedicines9020216Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the DiseasesSimone Patergnani0Esmaa Bouhamida1Sara Leo2Paolo Pinton3Alessandro Rimessi4Department of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, ItalyDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, ItalyDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, ItalyDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, ItalyDepartment of Medical Sciences and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, ItalyA decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate immune signaling cascades to intensify the inflammatory response at front of different stimuli. Here, we review the evidence that an exacerbation in the levels of mitochondrial-derived reactive oxygen species (ROS) contribute to mito-inflammation, a new concept that identifies the compartmentalization of the inflammatory process, in which the mitochondrion acts as central regulator, checkpoint, and arbitrator. In particular, we discuss how ROS contribute to specific aspects of mito-inflammation in different inflammatory-related diseases, such as neurodegenerative disorders, cancer, pulmonary diseases, diabetes, and cardiovascular diseases. Taken together, these observations indicate that mitochondrial ROS influence and regulate a number of key aspects of mito-inflammation and that strategies directed to reduce or neutralize mitochondrial ROS levels might have broad beneficial effects on inflammatory-related diseases.https://www.mdpi.com/2227-9059/9/2/216oxidative stressmitochondriamito-inflammationcancerpulmonary diseasesgastrointestinal disorders
spellingShingle Simone Patergnani
Esmaa Bouhamida
Sara Leo
Paolo Pinton
Alessandro Rimessi
Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the Diseases
Biomedicines
oxidative stress
mitochondria
mito-inflammation
cancer
pulmonary diseases
gastrointestinal disorders
title Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the Diseases
title_full Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the Diseases
title_fullStr Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the Diseases
title_full_unstemmed Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the Diseases
title_short Mitochondrial Oxidative Stress and “Mito-Inflammation”: Actors in the Diseases
title_sort mitochondrial oxidative stress and mito inflammation actors in the diseases
topic oxidative stress
mitochondria
mito-inflammation
cancer
pulmonary diseases
gastrointestinal disorders
url https://www.mdpi.com/2227-9059/9/2/216
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