Abstract
Wound healing and scar formation is a complex biological process that occurs as a response to injury, characterized by the deposition of extracellular matrix components and the proliferation of fibroblasts. The mechanisms underlying wound healing and following scar formation can vary significantly depending on the type of scar, such as hypertrophic scars and keloids, and are influenced by various cellular and molecular factors. Myofibroblasts, a differentiated form of fibroblasts, play a pivotal role in wound healing and scar formation due to their contractile properties and ability to produce large amounts of collagen and other extracellular matrix components. Scar formation process involves complex interactions among various cell types, including fibroblasts, macrophages, and endothelial cells, as well as the extracellular matrix components. Understanding these mechanisms is crucial for developing therapeutic strategies to minimize pathological scarring, such as hypertrophic scars and keloids. The initial phase of scar formation is dominated by inflammation, which is essential for initiating the healing process. Inflammatory cells, particularly macrophages, play a pivotal role in orchestrating the wound healing response. Fibroblasts are the primary effector cells in scar formation, responsible for synthesizing extracellular matrix components, including collagen. Scars can be classified into several types based on their characteristics, underlying mechanisms, and clinical presentations. The two most commonly discussed types of scars are hypertrophic scars and keloids, but there are also atrophic scars, contracture scars, and acne scars, each with distinct features and implications for treatment. The aim of this study is to explain the molecular mechanism, types and treatment of scar formation.
Published Version
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