Oxidative Stress and Tissue Repair: Mechanism, Biomarkers, and Therapeutics

摘要

During the “respiratory burst” in activated leukocytes, the release of reactive oxygen species (ROS) and reactive nitrogen species (RNS) occurs, and these phenomes present a central role in tissue repair [1, 2]. In the inflammatory phase, neutrophils reach the injured area, sending signals for the migration of macrophages that mediate the expression of cytokines, growth factors, reactive oxygen (ROS), and nitrogen species (RNS) [3]. These ROS and RNS generated during inflammation can lead to cell lesions such as membrane disorganization and protein oxidation by altering cellular functions. The balance between ROS production and antioxidant defense is important for efficient tissue repair in organs such as the skin, liver, lungs, kidneys, heart, and testes [4–6]. When the tissue is damaged by reactive species, it is common to observe lipid, protein, and DNA damage, leading to oxidative stress that disables tissue repair [5, 6].