In wound healing, what is the role of vascular endothelial growth factor (VEGF)?

Prepare for the Tissue Injury, Healing, and Pain Test. Utilize flashcards and multiple-choice questions with hints and explanations. Ensure you're ready for the exam!

Multiple Choice

In wound healing, what is the role of vascular endothelial growth factor (VEGF)?

VEGF is the main driver of new blood vessel formation during wound healing. It binds to receptors on endothelial cells, stimulating their proliferation, migration, and organization into new capillaries within the granulation tissue. This angiogenesis is essential to supply oxygen and nutrients needed for repair and to support the activity of other cells, including fibroblasts, during healing. VEGF also increases vascular permeability to allow plasma proteins to enter the tissue and help form a provisional matrix, which supports cellule and capillary growth. The other options don’t fit VEGF’s role: it does not inhibit fibroblast activity (fibroblasts are mainly influenced by growth factors like TGF-β and PDGF), it does not directly degrade the extracellular matrix (that task is carried out by matrix metalloproteinases and other proteases), and it does not suppress inflammation (VEGF can be associated with inflammatory signaling and increases in permeability rather than acting as an anti-inflammatory agent).

VEGF is the main driver of new blood vessel formation during wound healing. It binds to receptors on endothelial cells, stimulating their proliferation, migration, and organization into new capillaries within the granulation tissue. This angiogenesis is essential to supply oxygen and nutrients needed for repair and to support the activity of other cells, including fibroblasts, during healing. VEGF also increases vascular permeability to allow plasma proteins to enter the tissue and help form a provisional matrix, which supports cellule and capillary growth.

The other options don’t fit VEGF’s role: it does not inhibit fibroblast activity (fibroblasts are mainly influenced by growth factors like TGF-β and PDGF), it does not directly degrade the extracellular matrix (that task is carried out by matrix metalloproteinases and other proteases), and it does not suppress inflammation (VEGF can be associated with inflammatory signaling and increases in permeability rather than acting as an anti-inflammatory agent).

More practice questions