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Journals
Antioxidants
Special Issues
The OxInflammation Process and Tissue Repair
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The OxInflammation Process and Tissue Repair

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: 20 October 2024 | Viewed by 606

Special Issue Editors

Prof. Dr. Reggiani Vilela Gonçalves

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Guest Editor
Animal Biology Department, Federal University of Viçosa, Viçosa 36570-900, Minas Gerais, Brazil
Interests: oxidative stress; inflammation process; tissue repair; skin diseases; inflammatory process; biotechnologies
Special Issues, Collections and Topics in MDPI journals
Dr. Mariaurea Matias Sarandy

E-Mail Website
Guest Editor
Plants for Human Health Institute, North Carolina State University (NCSU), Kannapolis, NC 28081, USA
Interests: wound healing; natural product; oxidative profile; inflammatory markers; cell culture; histopathological processes; cellular and molecular mechanisms
Prof. Dr. Rômulo Dias Novaes

E-Mail Website
Guest Editor
Biomedical Science Department, Federal University of Alfenas, Alfenas 37130-001, Minas Gerais, Brazil
Interests: morphology; molecular biology; cardiovascular system; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Excessive ROS production inhibits cell migration and proliferation, affecting the expression and function of anti-inflammatory mediators. This effect enhances the inflammatory process, showing positive feedback among inflammatory and oxidative pathways, known as the OxInflammation process. During the normal wound healing process, there is an expression of many antioxidant genes, such as glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD), that are involved in the antioxidant defense network. Antioxidant enzymes limit the excessive production of ROS, inhibiting the expression and activity of pro-inflammatory mediators such as COX-2 and iNOS, and attenuating the production of ROS. However, the negative regulation of these antioxidant genes results in a delay in the healing process, and the excess ROS generated during inflammation can lead to cell damage, such as membrane rupture, DNA damage and protein oxidation. By altering cellular functions, oxidative stress is induced, thus inhibiting cell migration and proliferation, and affecting the expression and function of inflammatory mediators. Without sufficient antioxidant activity, wound healing can be delayed or severe tissue damage can occur. In this issue, we propose to investigate the direct interaction between the cellular and molecular mechanisms involved in tissue regeneration and maintenance of homeostasis. In addition, we aim to understand the biochemical signals, ligand–receptor interactions and molecular pathways, as well as the activation of alternative pathways that have shown significant relevance in modulating tissue reorganization in preclinical and clinical models. In this context, this issue proposes an update on different biological regulators in regenerative medicine, providing direction for developing current and future therapies. This Special Issue aims to create an interdisciplinary platform involving morphological, physiological, biochemical, molecular, pathological and biotechnological issues to discuss the identification, relevance and updates in the OxInflammation process and tissue repair. We welcome primary research articles (in silico, in vitro and in vivo) and secondary studies (critical integrative and systematic reviews) that will illustrate and stimulate the continuing effort to understand the relationship between oxidative stress and inflammation processes in the repair of different morphological and/or functional disorders of target organs caused by physical, chemical, biological and/or genetic processes.

Prof. Dr. Reggiani Vilela Gonçalves
Dr. Mariaurea Matias Sarandy
Prof. Dr. Rômulo Dias Novaes
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

  • oxidative stress
  • inflammasome
  • cytokines
  • angiogenesis
  • molecular biology
  • cellular and molecular mechanisms
  • diabetes
  • tissue repair

Published Papers (1 paper)

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23 pages, 4550 KiB  
Systematic Review
OxInflammatory Responses in the Wound Healing Process: A Systematic Review
by Fernanda Barbosa Lopes, Mariáurea Matias Sarandy, Rômulo Dias Novaes, Giuseppe Valacchi and Reggiani Vilela Gonçalves
Antioxidants 2024, 13(7), 823; https://doi.org/10.3390/antiox13070823 - 9 Jul 2024
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Abstract
Significant sums are spent every year to find effective treatments to control inflammation and speed up the repair of damaged skin. This study investigated the main mechanisms involved in the skin wound cure. Consequently, it offered guidance to develop new therapies to control [...] Read more.
Significant sums are spent every year to find effective treatments to control inflammation and speed up the repair of damaged skin. This study investigated the main mechanisms involved in the skin wound cure. Consequently, it offered guidance to develop new therapies to control OxInflammation and infection and decrease functional loss and cost issues. This systematic review was conducted using the PRISMA guidelines, with a structured search in the MEDLINE (PubMed), Scopus, and Web of Science databases, analyzing 23 original studies. Bias analysis and study quality were assessed using the SYRCLE tool (Prospero number is CRD262 936). Our results highlight the activation of membrane receptors (IFN-δ, TNF-α, toll-like) in phagocytes, especially macrophages, during early wound healing. The STAT1, IP3, and NF-kβ pathways are positively regulated, while Ca2+ mobilization correlates with ROS production and NLRP3 inflammasome activation. This pathway activation leads to the proteolytic cleavage of caspase-1, releasing IL-1β and IL-18, which are responsible for immune modulation and vasodilation. Mediators such as IL-1, iNOS, TNF-α, and TGF-β are released, influencing pro- and anti-inflammatory cascades, increasing ROS levels, and inducing the oxidation of lipids, proteins, and DNA. During healing, the respiratory burst depletes antioxidant defenses (SOD, CAT, GST), creating a pro-oxidative environment. The IFN-δ pathway, ROS production, and inflammatory markers establish a positive feedback loop, recruiting more polymorphonuclear cells and reinforcing the positive interaction between oxidative stress and inflammation. This process is crucial because, in the immune system, the vicious positive cycle between ROS, the oxidative environment, and, above all, the activation of the NLRP3 inflammasome inappropriately triggers hypoxia, increases ROS levels, activates pro-inflammatory cytokines and inhibits the antioxidant action and resolution of anti-inflammatory cytokines, contributing to the evolution of chronic inflammation and tissue damage. Full article
(This article belongs to the Special Issue The OxInflammation Process and Tissue Repair)
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