Editorial
Copyright ©The Author(s) 2025.
World J Biol Chem. Jun 5, 2025; 16(2): 107195
Published online Jun 5, 2025. doi: 10.4331/wjbc.v16.i2.107195
Table 1 Mechanisms and factors by which platelet-rich fibrin facilitates wound healing
Mechanism/factor
Details
Role in wound healing
Signaling molecules/cytokines/chemokines
Fibrin matrix formationPRF forms a dense fibrin matrixProvides a structural scaffold for cell migration and proliferation. Traps and concentrates GFs and signaling molecules at the wound site
Sustained release of GFsPRF allows for the gradual and sustained release of GFsProlonged stimulation of tissue repair mechanisms. Supports cellular proliferation, differentiation, and migrationPDGF, TGF-β, VEGF
Modulation of inflammationPRF helps regulate the inflammatory responsePrevents excessive or prolonged inflammation, promoting a balanced healing environmentMay involve modulation of pro-inflammatory cytokines (tumor necrosis factor-alpha, interleukin-1) and anti-inflammatory mediators
Enhanced cell migration and proliferationGFs released from PRF stimulate cell migration and proliferationAccelerates tissue regeneration and wound closurePDGF, TGF-β, and other GFs stimulate cellular signaling pathways involved in cell migration (e.g., Rho GTPases) and proliferation (mitogen-activated protein kinases/extracellular signal-regulated kinase)
Promotion of collagenizationPRF supports collagen deposition and organizationContributes to the structural remodeling of the wound matrix and enhances long-term tissue strengthTGF-β plays a key role in stimulating collagen synthesis by fibroblasts
AngiogenesisPRF promotes the formation of new blood vesselsImproves blood supply to the wound, delivering oxygen and nutrients necessary for healingVEGF stimulates signaling pathways involved in endothelial cell proliferation and migration (such as VEGF-R signaling)
Matrix remodelingPRF influences the remodeling of the extracellular matrixContributes to the restoration of functional tissue and minimizes scar formationInvolves matrix metalloproteinases and their inhibitors