Inflammatory response in wound tissue

The inflammatory response in wound tissue is a coordinated, transient process involving the recruitment and activation of immune cells (neutrophils, monocytes/macrophages, lymphocytes) and the release of cytokines and chemokines, which serve to clear pathogens, remove debris, and initiate tissue repair. Dysregulation or prolongation of this response can result in chronic, non-healing wounds, excessive scarring, or pathological fibrosis. Molecular targets within this process include chemokines (e.g., CCL2), cytokines (e.g., IL-1β, TNF-α), cellular receptors (e.g., CXCR2), transcription factors (e.g., NF-κB, Nrf2), and proteins involved in apoptosis (e.g., caspases). However, "inflammatory response in wound tissue" is not a single protein or receptor, but a description of the active phase of immune system engagement after tissue injury[1][2][3][4][5].\n\nThis term does not refer to a molecule, receptor, or gene, but instead describes a phase of the wound healing process regulated by many molecules and signaling pathways—each of which may individually represent true drug targets. For structured target information, it is necessary to specify one of these molecules (for example, "Interleukin-1 beta", "Tumor necrosis factor alpha", or "C-X-C motif chemokine receptor 2").

Other names

Wound inflammationInflammation in wound healingInflammatory phase of wound repair