Paracrine modulation of skin wound healing via secreted growth factors and cytokines

Paracrine modulation of skin wound healing involves a complex interplay of growth factors and cytokines secreted by various cell types to coordinate tissue repair. This process is essential for transitioning through the inflammatory, proliferative, and remodeling phases of healing (Werner & Grose, 2003). Key signaling molecules include Platelet-Derived Growth Factor (PDGF), Fibroblast Growth Factor (FGF), and Transforming Growth Factor-beta (TGF-β), which act on adjacent cells to promote migration and extracellular matrix production (Barrientos et al., 2008). Vascular Endothelial Growth Factor (VEGF) is also critical for stimulating angiogenesis within the wound bed to restore blood supply. In chronic wounds, such as diabetic foot ulcers, this paracrine signaling is often impaired, leading to a persistent inflammatory state and failure to close (Behm et al., 2012). Drugs like Becaplermin (recombinant PDGF) are used clinically to supplement these factors and promote healing in chronic ulcers. However, the therapeutic use of growth factors faces challenges such as rapid degradation by proteases in the wound environment and the need for localized delivery. There are also safety concerns regarding the potential for excessive tissue fibrosis or the promotion of neoplastic growth if signaling is not properly controlled.

Other names

Paracrine signaling in wound repairGrowth factor-mediated wound healingCytokine-mediated wound healing

Activation of specific cell surface receptors (e.g., PDGFR, FGFR, VEGFR) on target cells to initiate signaling pathways such as MAPK/ERK and PI3K/Akt, which drive cellular responses necessary for tissue repair.