Growth factor receptors involved in wound healing (RTKs)

This target group comprises several families of receptor tyrosine kinases (RTKs), including Platelet-Derived Growth Factor Receptors (PDGFR), Vascular Endothelial Growth Factor Receptors (VEGFR), and Epidermal Growth Factor Receptors (EGFR), which are essential mediators of the wound healing process. These receptors facilitate cellular responses such as proliferation, migration, and the formation of new blood vessels (angiogenesis) in response to tissue injury (PMID: 23991618). In a physiological context, they coordinate the complex interplay between fibroblasts, endothelial cells, and keratinocytes to restore tissue integrity. However, in oncology, these pathways are frequently co-opted by tumors to support uncontrolled growth and metastasis, making them primary targets for anti-angiogenic and anti-proliferative therapies (PMID: 15156151). Therapeutic strategies include small-molecule tyrosine kinase inhibitors (TKIs) like sunitinib and monoclonal antibodies like bevacizumab that neutralize circulating ligands. Because these receptors are vital for normal vascular homeostasis and tissue repair, their systemic inhibition can lead to significant adverse effects such as hypertension, hemorrhage, and, paradoxically, impaired wound healing (PMID: 19073455). Clinical management often requires balancing the efficacy of these drugs against their potential for cardiovascular and gastrointestinal toxicity.

Other names

Receptor tyrosine kinasesAngiogenic growth factor receptorsMitogenic receptorsPlatelet-derived growth factor receptorVascular endothelial growth factor receptorEpidermal growth factor receptorFibroblast growth factor receptor

Competitive inhibition of the ATP-binding site within the intracellular tyrosine kinase domain or monoclonal antibody-mediated neutralization of extracellular ligands to block downstream signaling pathways such as MAPK/ERK and PI3K/Akt.