Oxidative Stress and Tissue Repair: Mechanism, Biomarkers, and Therapeutics
1Federal University of Viçosa, Viçosa, Brazil
2State University of Rio de Janeiro, Rio de Janeiro, Brazil
3Freie Universitat Berlin, Berlin, Germany
Oxidative Stress and Tissue Repair: Mechanism, Biomarkers, and Therapeutics
Description
Tissue repair is a complex process that occurs after tissue damage and usually involves three stages: inflammation, proliferation, and remodeling. In each of these stages, different cells migrate to the wound area in order to provide protection and mediate the expression of pro- and anti-inflammatory proteins. Neutrophils are the first cells to arrive in the injured area, sending redox signals, histamine, bradykinin, and thrombin that increases vascular permeability and promotes the migration of macrophages that mediate the expression of cytokines, growth factors, reactive oxygen species (ROS), and reactive nitrogen species (RNS). These ROS and RNS generated during inflammation can lead to cell membrane disorganization and protein oxidation by altering the cellular function. Therefore, the balance between ROS production and antioxidant defenses is important for efficient tissue repair in organs such as skin, liver, lungs, kidneys, heart, and testes. An increased oxygen consumption occurs during the process of tissue repair, resulting in an intense production of ROS and RNS. When the tissue is damaged by reactive species, it is common to observe lipid, protein, and DNA damage, leading to oxidative stress that impairs tissue repair.
Regarding the pivotal role played by antioxidant defenses in maintaining the morphological and functional integrity during tissue repair, the development of new drugs with antioxidant properties has been shown to be potentially useful in accelerating tissue recovery. These new drugs act by increasing enzymatic and nonenzymatic antioxidant defenses, protecting against ROS and RNS and attenuating the formation of biomarkers such as malondialdehyde, hydroperoxides, nitric oxide, and carbonyl protein at tissue level. This antioxidant activity might favor tissue repair, thus contributing to tissue protection and accelerating the healing process. In addition, treatments that increase levels of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and gluthatione-peroxidase (GPx) are shown to accelerate the healing process in different tissues. In this process, antioxidant molecules are potentially beneficial as they stimulate fibroblast migration and proliferation and increase collagen synthesis and scar tensile strength, a process partially mediated by ROS and RNS catalysis.
Accordingly, evidence from preclinical (in vitro and in vivo) and clinical studies opens new perspectives for development of pharmacological strategies to accelerate tissue repair. These therapies usually stimulate the synthesis of antioxidant proteins and accelerate the completion of the inflammatory process, as well as decreasing the oxidative stress in regenerating tissues.
This special issue aims to create an interdisciplinary platform involving morphological, physiological, and pathological issues to discuss the cellular and molecular basis of the metabolism redox associated with repair tissue. We welcome primary research articles (in silico, in vitro, and in vivo), as well as comprehensive and systematic review articles, that will illustrate and stimulate the continuing effort to understand the redox systems in tissue repair metabolism, biomarkers, and treatments.
Potential topics include but are not limited to the following:
- Metabolism redox in tissue repair
- Biomarkers of oxidative stress and antioxidant defenses during tissue repair
- Therapies that act as antioxidants during the repair process
- Analytical methods and instrumentation applied to the analysis of redox metabolism in tissue repair
- Redox mechanisms involved in inflammatory processes during tissue repair
- Redox mechanisms involved in regeneration and tissue healing processes