The OxInflammation Process and Tissue Repair

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

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