Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases III

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: 30 April 2024 | Viewed by 1439

Special Issue Editors


E-Mail Website
Guest Editor
Department of Cell Death and Proliferation, Institut D'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas (IIBB-CSIC), Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), 08036 Barcelona, Spain
Interests: liver diseases; nafld; liver fibrosis; nkt cells; liver immunology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Cell Death and Proliferation, Institut D'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas (IIBB-CSIC), Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), 08036 Barcelona, Spain
Interests: Alzheimer’s disease; cholesterol in neurodegeneration; mitochondria; mitochondrial oxidative stress; autophagy/mitophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although necessary for life, mitochondria are often essential for initiating apoptotic death and deciding cell fate under cellular stress. Recently, in addition to their role in cell death, mitochondria have been suggested to serve as signaling platforms critical for regulating autophagy and the inflammatory response. Mitochondrial oxidative/nitrosative stress has been reported to trigger autophagy by promoting autophagosome formation and induce the release of inflammatory cytokines through the activation of the NLRP3-inflammasome. Thus, it is becoming clear that mitochondria participate in many aspects of cell function, and evidence further suggests that mitochondria impairment is underlying many common human disorders. Consequently, new strategies are being sought to restore the mitochondrial function therapeutically.

Contributions to this Special Issue may cover research findings or review articles related to the role of mitochondrial oxidative stress and mitochondrial dysfunction in different pathological conditions ranging from cancer to neurodegenerative diseases, the mechanistic links between changes in mitochondria functionality and alterations of cellular processes such as autophagy and the inflammatory signaling pathways and its impact on cell viability, and the use of mitochondria-targeted molecules, including antioxidants, as therapeutic strategies for disease intervention.

Dr. Montserrat Marí
Dr. Anna Colell
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondrial oxidative stress
  • autophagy
  • mitophagy
  • inflammasome
  • antioxidants
  • mitochondrial dysfunction
  • mitochondrial-targeted molecules
  • disease

Related Special Issues

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

15 pages, 2226 KiB  
Article
Mitochondrial Stress Links Environmental Triggers with Pro-Inflammatory Signaling in Crohn’s Disease
by Flores Martín-Reyes, Manuel Bernal, Cristina Rodríguez-Díaz, Damaris Rodríguez-de los Reyes, Ailec Ho-Plagaro, Francisca Rodríguez-Pacheco, Laura Camacho-Martel, Raquel Camargo-Camero, Francisco J. Rodríguez-González, Guillermo Alcain-Martínez, Rafael Martín-Masot, Víctor M. Navas-López, Marina Villanueva-Paz, María Isabel Lucena, Eduardo García-Fuentes and Carlos López-Gómez
Antioxidants 2023, 12(12), 2105; https://doi.org/10.3390/antiox12122105 - 13 Dec 2023
Viewed by 1045
Abstract
Inflammatory Bowel Diseases (IBD) are a group of chronic, inflammatory disorders of the gut. The incidence and activity of IBD are determined by both genetic and environmental factors. Among these factors, polymorphisms in genes related to autophagy and the consumption of non-steroidal anti-inflammatory [...] Read more.
Inflammatory Bowel Diseases (IBD) are a group of chronic, inflammatory disorders of the gut. The incidence and activity of IBD are determined by both genetic and environmental factors. Among these factors, polymorphisms in genes related to autophagy and the consumption of non-steroidal anti-inflammatory drugs (NSAIDs) have been consistently associated with IBD. We show that NSAIDs induce mitochondrial stress and mitophagy in intestinal epithelial cells. In an altered mitophagy context simulating that observed in IBD patients, NSAID-induced mitochondrial stress leads to the release of mitochondrial components, which act as Danger Associated Molecular Patterns with pro-inflammatory potential. Furthermore, colonic organoids from Crohn’s disease patients and healthy donors show activation of the mitochondrial Unfolded Protein Response (UPRmt) upon treatment with ibuprofen. Finally, colon biopsies from Crohn’s disease patients in remission or with low-to-moderate activity also show expression of genes involved in UPRmt, while patients with severe activity show no increase compared to healthy donors. Our results suggest the involvement of mitochondria in the mechanisms triggering inflammation in IBD after NSAID use. Moreover, our results highlight the clinical relevance of mitochondrial stress and activation of the UPRmt pathway in the pathophysiology of Crohn’s disease. Full article
Show Figures

Graphical abstract

Back to TopTop