Keloids are chronic inflammatory fibroproliferative disorders characterized by invasive growth beyond the original wound margins and a high recurrence rate, substantially impairing patients’ quality of life. Their pathogenesis is complex and arises from the synergistic interplay among the mechanical microenvironment, chronic inflammation, and profibrotic signaling networks.
The inflammatory and proliferative phases of normal wound healing are pathologically prolonged, with sustained activation of fibroblasts and myofibroblasts, resulting in excessive extracellular matrix (ECM) deposition and aberrant remodeling. Within the immune microenvironment, infiltrating M2 macrophages and Th2/Th17 cells, among others, secrete a broad array of cytokines, thereby establishing a chronic inflammatory circuit.
Mechanical forces act as a pivotal driving factor: stress concentration in high-tension regions and activation of fibroblast mechanotransduction pathways (e.g., Hippo–YAP/TAZ and integrin–FAK) interact with inflammatory responses to form a self-amplifying “mechanical force–inflammation–fibrosis” positive feedback loop, exacerbating disease progression. Current management primarily relies on multimodal regimens such as surgery combined with radiotherapy and intralesional pharmacologic injections, yet remains challenged by high recurrence rates and marked heterogeneity.
Frontiers in Immunology published a clinical update in Infectious Disease on 24 Apr 2026.
The item focuses on Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.
Review the original article for the full source wording and details.