Authors : Prabhakar Singh Patel, Dr. Sameera Raini, Shambhavi Srivastava
DOI : 10.46376/GNJI/8.I.2025.772-774
Volume : 8
Issue : 1
Year : 2025
Page No : 772-774
A complex biological process, wound healing involves the coordinated interaction of molecular and cellular systems. It is an essential physiological reaction that guarantees tissue integrity after damage. Many variables, such as immune cells, extracellular matrix components, and inflammatory mediators, strictly regulate the process. Initiating tissue repair, attracting immune cells, and avoiding infections all depend on the early inflammatory response. However, whether wound healing occurs optimally or is hampered depends on the degree and duration of inflammation. By coordinating immune responses, tissue healing, and remodeling, inflammatory mediators are essential in controlling this process. These mediators, which each have a distinct role in different phases of healing, include cytokines, chemokines, growth factors, reactive oxygen species (ROS), and nitric oxide (NO). Early immune responses are triggered by pro-inflammatory mediators like tumor necrosis factor-alpha (TNF-α) and interleukin-1? (IL-1β), whereas anti-inflammatory mediators like interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β) aid in the wound's transition from the inflammatory to the repair phases. OneThis study examines the available data about the function of inflammatory mediators in wound healing, highlighting how they can both aid and hinder the healing process. While efficient repair requires acute inflammation, chronic wounds, fibrosis, and delayed healing can result from excessive or protracted inflammation. Successful healing outcomes thus depend on the delicate balance between pro-inflammatory and anti-inflammatory mediators.