Skin wound healing is a complex, dynamic process involving multiple stages and cellular mechanisms. The healing process begins with hemostasis and the formation of a provisional wound matrix, followed by an inflammatory phase, proliferation, and remodeling. During the inflammatory phase, neutrophils and monocytes are recruited to the wound site, initiating the immune response. The proliferative phase focuses on reepithelialization, granulation tissue formation, and neovascularization. Granulation tissue is characterized by high fibroblast density and is eventually replaced by mature, avascular tissue during the remodeling phase. Scar formation is a natural outcome of wound healing, influenced by the extent of inflammation. In contrast, fetal wound healing is unique in that it often results in scarless repair due to differences in the extracellular matrix, inflammatory response, and cellular mediators. Fetal skin has the ability to regenerate without scarring, with the process involving the regeneration of a collagen matrix and the healing of dermal appendages. However, in adults, wound healing typically results in scarring, which can lead to hypertrophic or keloid scars. Excessive scarring is associated with chronic inflammation, abnormal collagen maturation, and impaired apoptosis. Understanding the molecular and cellular mechanisms of wound healing is crucial for developing effective therapies to improve healing outcomes and reduce scarring. Research continues to uncover the complex interplay of cells, growth factors, and cytokines in wound healing, offering new insights into the development of advanced wound care strategies.Skin wound healing is a complex, dynamic process involving multiple stages and cellular mechanisms. The healing process begins with hemostasis and the formation of a provisional wound matrix, followed by an inflammatory phase, proliferation, and remodeling. During the inflammatory phase, neutrophils and monocytes are recruited to the wound site, initiating the immune response. The proliferative phase focuses on reepithelialization, granulation tissue formation, and neovascularization. Granulation tissue is characterized by high fibroblast density and is eventually replaced by mature, avascular tissue during the remodeling phase. Scar formation is a natural outcome of wound healing, influenced by the extent of inflammation. In contrast, fetal wound healing is unique in that it often results in scarless repair due to differences in the extracellular matrix, inflammatory response, and cellular mediators. Fetal skin has the ability to regenerate without scarring, with the process involving the regeneration of a collagen matrix and the healing of dermal appendages. However, in adults, wound healing typically results in scarring, which can lead to hypertrophic or keloid scars. Excessive scarring is associated with chronic inflammation, abnormal collagen maturation, and impaired apoptosis. Understanding the molecular and cellular mechanisms of wound healing is crucial for developing effective therapies to improve healing outcomes and reduce scarring. Research continues to uncover the complex interplay of cells, growth factors, and cytokines in wound healing, offering new insights into the development of advanced wound care strategies.