Wound healing is a complex, tightly regulated process that restores tissue structure and function after injury. It unfolds in overlapping stages: hemostasis, inflammation, proliferation and remodeling.

Hemostasis starts immediately as blood vessels constrict and platelets form a clot. This fibrin mesh stops bleeding and creates a scaffold for incoming cells. Inflammation follows within hours. Neutrophils and macrophages migrate into the wound, clearing microbes and debris while releasing signaling molecules that coordinate subsequent repair.

During the proliferative phase, new tissue forms. Fibroblasts deposit collagen and other matrix components, endothelial cells build new blood vessels and keratinocytes migrate across the wound surface to re establish the epidermis. Growth factors such as TGF beta, VEGF and PDGF are key regulators of cell proliferation, migration and angiogenesis in this phase.

In the remodeling phase, which can last months, the collagen network is reorganized and strengthened. Type III collagen laid down early is gradually replaced by type I collagen. The scar becomes more structured and less cellular, although it never fully regains the mechanical properties of uninjured skin.

Research highlights how oxygen supply, immune responses, microbiome composition, aging, diabetes and vascular disease can each disturb these stages and lead to chronic, non healing wounds. Such wounds often remain stuck in prolonged inflammation with impaired angiogenesis and defective matrix remodeling.

Current directions in wound healing research include bioengineered dressings that provide moisture and antimicrobial activity, scaffolds that mimic extracellular matrix, controlled release of growth factors, cell based therapies using stem or progenitor cells and strategies to modulate immune responses and microbiota to restore a balanced healing environment.