Keloids are benign fibroproliferative tumors characterized physically by hyalinized collagen and tongue-like advancing edges. Their pathogenesis is multifactorial, driven by inflammation, skin tension, and genetic susceptibility. While systemic Th2 cytokines (IL-4, IL-13) are often elevated, targeting this pathway with dupilumab has yielded conflicting clinical results, suggesting a complex immunological landscape. Mechanobiological studies indicate that high skin tension drives specific growth patterns (e.g., butterfly or dumbbell shapes) through mechanosensitive pathways and epigenetic regulation. Recent single-cell RNA sequencing (scRNA-seq) has unraveled significant cellular heterogeneity within keloid tissue. Notably, we highlight the role of Schwann cells, which secrete IGFBP5 and interact with M2 macrophages to promote extracellular matrix deposition and inflammation. Furthermore, scRNA-seq analysis of combination therapies, such as intralesional triamcinolone and 5-fluorouracil, reveals distinct regulatory changes in fibroblast and vascular endothelial cell lineages. This presentation synthesizes these molecular insights to propose optimized therapeutic algorithms for the precision management of pathological scars.

Download