This review discusses the mechanisms and therapies for scarring skin. Skin injuries in adults often result in fibrotic, non-functional scars. While multiple factors contribute to scar formation, the precise mechanisms remain unclear. The review explores the wound healing process, factors driving skin cells toward a scarring fate, and the impact of fibroblast heterogeneity on scar formation. Potential therapeutic interventions for scarring wounds are also discussed. Skin injuries, including burns, wounds, surgery, and infections, lead to scars. Scars can be categorized into four types: mature, immature, hypertrophic, and keloid. Hypertrophic scars are characterized by a bulging appearance, while keloids extend beyond the original wound and continue to enlarge. These scars differ histologically, with keloids showing irregular collagen accumulation. Scar formation is a complex process involving multiple cells, cytokines, and factors. Fibroblast heterogeneity significantly influences scar formation. The review outlines the wound healing process, which includes hemostasis/inflammation, proliferation, and remodeling. During the proliferative stage, keratinocytes and fibroblasts migrate and contribute to tissue repair. Fibroblasts generate contractile forces and participate in collagen production, which is crucial for ECM remodeling. Genetic factors, age, and sex influence scar formation. Genetic predisposition, DNA methylation, and histone acetylation play roles in keloid development. Age affects scar formation, with fetal skin regenerating without scarring, while adult skin forms scars. Gender also influences scar formation, with females more prone to pathological scars. Fibroblast heterogeneity is crucial in scar formation. Myofibroblasts, derived from various sources, play a key role in scar formation. Different fibroblast subtypes, such as SMA+ fibroblasts, ADAM12+ fibroblasts, POSTN+ fibroblasts, and Engrailed-1+ fibroblasts, contribute to scar formation through distinct mechanisms. Inflammation, particularly TGF-β and type 2 cytokines like IL-4 and IL-13, drives scar formation. TGF-β1 is a key regulator of myofibroblast activation and scar formation. IL-4 and IL-13 upregulate periostin, which in turn promotes TGF-β1 secretion, exacerbating scar formation. Therapeutic strategies for scar management include targeting TGF-β signaling, inhibiting fibroblast hyperproliferation, and modulating collagen metabolism. Corticosteroids, nonsteroidal anti-inflammatory drugs, and surgical interventions are also used. Mesenchymal stem cells and physical therapies like pressure therapy and silicone-based materials are promising approaches. The review highlights the need for further research into scarless wound healing and the development of novel therapies to reduce scarring. Understanding fibroblast heterogeneity and the mechanisms of fetal skin regeneration could lead to effective scarlessThis review discusses the mechanisms and therapies for scarring skin. Skin injuries in adults often result in fibrotic, non-functional scars. While multiple factors contribute to scar formation, the precise mechanisms remain unclear. The review explores the wound healing process, factors driving skin cells toward a scarring fate, and the impact of fibroblast heterogeneity on scar formation. Potential therapeutic interventions for scarring wounds are also discussed. Skin injuries, including burns, wounds, surgery, and infections, lead to scars. Scars can be categorized into four types: mature, immature, hypertrophic, and keloid. Hypertrophic scars are characterized by a bulging appearance, while keloids extend beyond the original wound and continue to enlarge. These scars differ histologically, with keloids showing irregular collagen accumulation. Scar formation is a complex process involving multiple cells, cytokines, and factors. Fibroblast heterogeneity significantly influences scar formation. The review outlines the wound healing process, which includes hemostasis/inflammation, proliferation, and remodeling. During the proliferative stage, keratinocytes and fibroblasts migrate and contribute to tissue repair. Fibroblasts generate contractile forces and participate in collagen production, which is crucial for ECM remodeling. Genetic factors, age, and sex influence scar formation. Genetic predisposition, DNA methylation, and histone acetylation play roles in keloid development. Age affects scar formation, with fetal skin regenerating without scarring, while adult skin forms scars. Gender also influences scar formation, with females more prone to pathological scars. Fibroblast heterogeneity is crucial in scar formation. Myofibroblasts, derived from various sources, play a key role in scar formation. Different fibroblast subtypes, such as SMA+ fibroblasts, ADAM12+ fibroblasts, POSTN+ fibroblasts, and Engrailed-1+ fibroblasts, contribute to scar formation through distinct mechanisms. Inflammation, particularly TGF-β and type 2 cytokines like IL-4 and IL-13, drives scar formation. TGF-β1 is a key regulator of myofibroblast activation and scar formation. IL-4 and IL-13 upregulate periostin, which in turn promotes TGF-β1 secretion, exacerbating scar formation. Therapeutic strategies for scar management include targeting TGF-β signaling, inhibiting fibroblast hyperproliferation, and modulating collagen metabolism. Corticosteroids, nonsteroidal anti-inflammatory drugs, and surgical interventions are also used. Mesenchymal stem cells and physical therapies like pressure therapy and silicone-based materials are promising approaches. The review highlights the need for further research into scarless wound healing and the development of novel therapies to reduce scarring. Understanding fibroblast heterogeneity and the mechanisms of fetal skin regeneration could lead to effective scarless