This review aims to elucidate the intricate mechanisms of wound healing and scar formation, focusing on the role of fibroblast heterogeneity. Skin injuries, such as burns, wounds, surgeries, and infections, often result in fibrotic and non-functional scars, affecting both aesthetics and quality of life. The review categorizes scars into four types: mature, immature, hypertrophic, and keloid, each with distinct characteristics. Hypertrophic scars and keloids, characterized by excessive collagen deposition, are particularly challenging to manage. The process of wound healing is divided into three stages: hemostasis/inflammation, proliferation, and remodeling. During inflammation, immune cells release cytokines that recruit neutrophils, monocytes, and lymphocytes, which contribute to tissue repair. In the proliferation stage, keratinocytes and fibroblasts restore the epithelial barrier and generate granulation tissue, respectively. The remodeling stage involves the degradation and reorganization of collagen fibers to restore skin tensile strength. Multiple factors influence scar formation, including genetic predisposition, age, gender, and anatomical factors. Genetic factors, such as polymorphisms in TGFβ1 and TNFAIP6, and histone modifications, play crucial roles. Age-related changes in fibroblast populations, particularly the increase in Engrailed-1 positive fibroblasts (EPFs), contribute to scar formation. Gender differences, with females having a higher propensity for pathological scars, are also noted. Fibroblast heterogeneity is a key factor in scar formation. Fibroblasts can differentiate into myofibroblasts, which are responsible for excessive collagen production and scar formation. Specific subtypes of fibroblasts, such as SMA+ fibroblasts, ADAM12+ fibroblasts, POSTN+ fibroblasts, and Engrailed-1+ fibroblasts, exhibit distinct functions and contribute differently to scar development. Inflammation, regulated by cytokines like TGF-β, IL-4, and IL-13, plays a critical role in fibroblast activation and scar formation. TGF-β1, in particular, is a key regulator, promoting myofibroblast activation and collagen deposition. Other cytokines, such as IL-4 and IL-13, also contribute to scar formation by upregulating periostin expression and promoting collagen cross-linking. Therapeutic strategies for scar management include targeting TGF-β signaling, inhibiting fibroblast hyperproliferation, altering collagen metabolism, and modulating the inflammatory response. Direct interventions targeting specific fibroblast lineages and understanding fetal wound healing mechanisms offer promising avenues for scarless treatment. However, further research is needed to optimize these approaches and develop novel therapies for scar reduction and prevention.This review aims to elucidate the intricate mechanisms of wound healing and scar formation, focusing on the role of fibroblast heterogeneity. Skin injuries, such as burns, wounds, surgeries, and infections, often result in fibrotic and non-functional scars, affecting both aesthetics and quality of life. The review categorizes scars into four types: mature, immature, hypertrophic, and keloid, each with distinct characteristics. Hypertrophic scars and keloids, characterized by excessive collagen deposition, are particularly challenging to manage. The process of wound healing is divided into three stages: hemostasis/inflammation, proliferation, and remodeling. During inflammation, immune cells release cytokines that recruit neutrophils, monocytes, and lymphocytes, which contribute to tissue repair. In the proliferation stage, keratinocytes and fibroblasts restore the epithelial barrier and generate granulation tissue, respectively. The remodeling stage involves the degradation and reorganization of collagen fibers to restore skin tensile strength. Multiple factors influence scar formation, including genetic predisposition, age, gender, and anatomical factors. Genetic factors, such as polymorphisms in TGFβ1 and TNFAIP6, and histone modifications, play crucial roles. Age-related changes in fibroblast populations, particularly the increase in Engrailed-1 positive fibroblasts (EPFs), contribute to scar formation. Gender differences, with females having a higher propensity for pathological scars, are also noted. Fibroblast heterogeneity is a key factor in scar formation. Fibroblasts can differentiate into myofibroblasts, which are responsible for excessive collagen production and scar formation. Specific subtypes of fibroblasts, such as SMA+ fibroblasts, ADAM12+ fibroblasts, POSTN+ fibroblasts, and Engrailed-1+ fibroblasts, exhibit distinct functions and contribute differently to scar development. Inflammation, regulated by cytokines like TGF-β, IL-4, and IL-13, plays a critical role in fibroblast activation and scar formation. TGF-β1, in particular, is a key regulator, promoting myofibroblast activation and collagen deposition. Other cytokines, such as IL-4 and IL-13, also contribute to scar formation by upregulating periostin expression and promoting collagen cross-linking. Therapeutic strategies for scar management include targeting TGF-β signaling, inhibiting fibroblast hyperproliferation, altering collagen metabolism, and modulating the inflammatory response. Direct interventions targeting specific fibroblast lineages and understanding fetal wound healing mechanisms offer promising avenues for scarless treatment. However, further research is needed to optimize these approaches and develop novel therapies for scar reduction and prevention.