Wound healing is a process that requires a series of cellular and molecular interdependent events to restore tissue integrity after lesions. This process is mediated by growth factors, cytokines, resident and transitory cells, and is organized in phases involving inflammation, cell proliferation, and tissue remodeling. In the inflammatory phase, immune cells migrate to lesion areas to remove injured tissue and initiate the process of blood coagulation, which also promotes vascular hemostasis and releases chemotactic factors that stimulate the migration and activation of immune cells. In addition, during recovery of the injured area occurs leukocyte infiltration and releases proinflammatory cytokines, such as (IL1 and IL6), tumor necrosis factor-α and interferon gamma (IFN-γ).

Guided by these molecules, the proliferative stage progresses with intense cell proliferation and secretion of a provisory extra cellular matrix (ECM), covering the injured area with a highly vascularized and hydrated tissue. Apoptosis of most infiltrating leukocytes and down-regulation of pro-inflammatory mediators conduces to a remodeling process, which can evolve with tissue regeneration or healing. The remodeling phase corresponds mainly to changes in the extracellular matrix of the scar tissue, where most type III collagen fibers are progressively replaced by type I fibers, which are more resistant and abundant in intact skin.

Due to the complexity and interdependence of all phases of tissue repair, morphofunctional disturbances are not uncommon, especially when associated to metabolic (i.e., diabetes mellitus, vasculopathies) and microbial diseases (i.e., bacterial, fungal and parasitic infections). During inflammation, frequently cells release reactive oxygen (ROS) and nitrogen (RNS) species, which can lead to cell membrane disorganization and protein oxidation, consequently altering the cellular function. The balance between the production of pro-oxidant molecules and antioxidant effectors is important for efficient tissue repair. When the tissue is damaged, the inflammatory process triggers an intense production of radical and non-radical pro-oxidant mediators (i.e., OH•-, O2•-, H2O2, and NO), which are directly associated to lipid, protein and DNA oxidative damage that often culminates in disorganization of ECM and cell death. Therefore, a redox balance is necessary and contributes to create a molecular microenvironment favorable for stimulating fibroblast proliferation, migration, and activation, which culminates in adequate production and organization of ECM and a fast-wound closure.

This Special Issue aims to create an interdisciplinary platform involving morphological, physiological, biochemical, molecular, and pathological issues to discuss the relevance of the cellular and molecular mechanism of oxidative stress in wound healing. We welcome primary research articles and secondary studies that will illustrate and stimulate the continuing effort to understand the importance of cellular and molecular mechanisms in the repair of different morphological and/or functional disorders of target organs caused by physical, chemical, biological, and/or genetic processes.

Potential topics include but are not limited to the following:

• Metabolism redox in wound healing
• Biomarkers of oxidative stress and antioxidant defenses during wound healing
• Therapies that act as antioxidants during the repair process
• Analytical methods and instrumentation applied to the analysis of cell and molecular mechanisms in tissue repair
• Main redox mechanisms involved in inflammatory processes during wound healing