Hypertrophic scars and keloids are abnormal scarring conditions resulting from disrupted wound healing. They can cause pain, itching, and contractures, significantly affecting patients' quality of life. Despite extensive research, effective treatments remain limited due to a poor understanding of the underlying mechanisms. This review summarizes current knowledge of the pathophysiology of hypertrophic scars and keloids, discusses established treatments, and explores emerging therapeutic strategies. Hypertrophic scars develop within 4-8 weeks after injury and typically regress over years, while keloids may form years after minor injuries and persist without regression. Clinically, they differ in appearance and behavior, though differentiation can be challenging. Histologically, both contain excess collagen, but keloids have disorganized collagen and more myofibroblasts. Keloids are more common in darker-skinned individuals and have a genetic predisposition. The pathophysiology of excessive scar formation involves an imbalance between anabolic and catabolic processes, with prolonged inflammation and fibroblast activity contributing to keloid formation. TGF-β plays a key role, with its expression and signaling pathways being critical in both conditions. SMAD signaling, downstream of TGF-β, is involved in collagen synthesis and fibrosis. Emerging treatments include recombinant TGF-β3, which has shown promise in reducing scarring, and imiquimod, which may reduce keloid recurrence. Corticosteroid injections, cryotherapy, laser therapy, and surgical excision are established treatments, though recurrence rates remain a challenge. Other therapies, such as 5-FU and bleomycin, have shown efficacy in reducing scar size and symptoms. Despite advances, effective treatments for hypertrophic scars and keloids remain limited, with a need for further research into molecular mechanisms and novel therapeutic approaches. Current strategies focus on modulating inflammatory responses, fibroblast activity, and collagen synthesis to prevent or reduce excessive scarring.Hypertrophic scars and keloids are abnormal scarring conditions resulting from disrupted wound healing. They can cause pain, itching, and contractures, significantly affecting patients' quality of life. Despite extensive research, effective treatments remain limited due to a poor understanding of the underlying mechanisms. This review summarizes current knowledge of the pathophysiology of hypertrophic scars and keloids, discusses established treatments, and explores emerging therapeutic strategies. Hypertrophic scars develop within 4-8 weeks after injury and typically regress over years, while keloids may form years after minor injuries and persist without regression. Clinically, they differ in appearance and behavior, though differentiation can be challenging. Histologically, both contain excess collagen, but keloids have disorganized collagen and more myofibroblasts. Keloids are more common in darker-skinned individuals and have a genetic predisposition. The pathophysiology of excessive scar formation involves an imbalance between anabolic and catabolic processes, with prolonged inflammation and fibroblast activity contributing to keloid formation. TGF-β plays a key role, with its expression and signaling pathways being critical in both conditions. SMAD signaling, downstream of TGF-β, is involved in collagen synthesis and fibrosis. Emerging treatments include recombinant TGF-β3, which has shown promise in reducing scarring, and imiquimod, which may reduce keloid recurrence. Corticosteroid injections, cryotherapy, laser therapy, and surgical excision are established treatments, though recurrence rates remain a challenge. Other therapies, such as 5-FU and bleomycin, have shown efficacy in reducing scar size and symptoms. Despite advances, effective treatments for hypertrophic scars and keloids remain limited, with a need for further research into molecular mechanisms and novel therapeutic approaches. Current strategies focus on modulating inflammatory responses, fibroblast activity, and collagen synthesis to prevent or reduce excessive scarring.