Plastic Surgery

Immune-centric model of keloids opens door to targeted biologic therapy

This review reconceptualizes keloids as an immune-driven disease rather than a purely fibroblast-mediated scar. Single-cell and multi-omics studies show enrichment of M2 macrophages, mast cells, Th2/Th17 cells, and dendritic cells sustaining fibroblast activation and fibrosis. Key profibrotic circuits involve TGF-β/Smad, IL-4/IL-13, IL-6/JAK-STAT3, and PI3K/AKT/mTOR pathways interacting with mechanical stress. Soluble HLA-E and tissue-resident memory T cells are highlighted as potential biomarkers of progression and postoperative relapse. Early clinical experience with dupilumab shows reduced lesion burden and pruritus, and multiple cytokine and checkpoint targets are in exploration. Translation is limited by a lack of robust keloid models and large trials, reinforcing the need for immune profiling in high-risk patients. 1

Scaffold-free, collagen-guided adipose constructs to stabilize soft-tissue volume

This study reports a Self-Assembly Fat (SAF) construct derived from lipoaspirate via intrinsic type I collagen crosslinking. Exogenous collagen supplementation (SAF⁺) increased stiffness, elasticity, and cohesion while preserving handling for potential flap-like implantation. In vitro, SAF⁺ enhanced adipogenic differentiation and improved stem cell recruitment compared with unsupplemented constructs. In vivo, SAF⁺ accelerated soft-tissue repair by promoting M2 macrophage polarization, angiogenesis, and stem cell homing. Mechanistically, integrin α2β1–FAK/Src activation linked collagen network formation to a pro-regenerative microenvironment. 2

Silk fibroin injectable rejuvenates fibroblasts and ECM in aged skin models

This work evaluates silk fibroin (SF) as an injectable scaffold targeting fibroblast senescence in aged skin. SF supported fibroblast adhesion and proliferation while decreasing senescence-associated secretory phenotype factors and restoring a more functional cell state. It reduced reactive oxygen species and matrix metalloproteinase expression via modulation of the ROS–MAPK–AP-1–MMP axis, slowing collagen degradation. SF restored ECM homeostasis through a non-inflammatory mechanism, contrasting with traditional fillers that rely on inflammatory collagen induction. These properties position SF as a candidate next-generation filler combining structural support with anti-senescent, pro-regenerative signaling. 3