Decoding keloids: Single-cell heterogeneity, emerging role of adipocytes, molecular biomarkers, and therapeutic implications in skin of color.

Keloids are a chronic, refractory, wound-triggered fibroproliferative disorder characterized by fibroblast overproduction, excessive extracellular matrix deposition, persistent inflammation, and invasive growth beyond original wound boundaries. Although keloid risk is associated with numerous genetic loci and skin of color, keloid pathogenesis remains incompletely understood. Multiomic technologies have identified cell populations and signaling networks associated with keloid pathogenesis. Emerging evidence highlights adipocyte lipolysis, epigenetic regulation by microRNAs, and disrupted vitamin D signaling as modulators of tissue repair and fibrosis. Genetic studies further implicate heritable risk factors. Integration of these approaches offers insights and therapeutic opportunities for this prevalent, debilitating condition.