angiogeneesis

Angiogenesis is the process by which new blood vessels form from pre-existing vasculature. It is essential for normal development, reproduction, and wound healing, but can contribute to disease when dysregulated. Angiogenesis is distinct from vasculogenesis, which builds vessels de novo from endothelial progenitors.

In adults, angiogenesis is typically driven by tissue hypoxia or inflammatory cues that upregulate pro-angiogenic factors, notably vascular endothelial growth factor (VEGF) and fibroblast growth factors (FGF). Endothelial cells respond by degrading the basement membrane, proliferating, and migrating toward the stimulus to form sprouts. Sprouting angiogenesis is guided by VEGF gradients and regulated by Notch signaling, which coordinates tip and stalk cell behavior. A second form, intussusceptive angiogenesis, splits existing vessels by forming intraluminal tissue pillars.

Maturation requires stabilization by pericytes and smooth muscle cells, recruited by PDGF-BB and angiopoietins, along with TGF-β signaling. Oxygen sensing via HIF-1 links hypoxia to VEGF production, while endogenous anti-angiogenic factors help limit growth.

Physiologically, angiogenesis is vital for embryonic development, placental formation, endometrial remodeling, and tissue repair. Pathological angiogenesis drives cancer growth and metastasis, ocular neovascular diseases, and inflammatory conditions. The "angiogenic switch" describes the shift toward a pro-angiogenic state in tumors.

Therapeutically, anti-angiogenic strategies target VEGF signaling or endothelial proliferation, using antibodies such as bevacizumab, VEGF traps, or multi-kinase inhibitors like sunitinib and sorafenib. Treatments aim to inhibit vessel formation or normalize abnormal vasculature. Assessments rely on imaging and histological measures such as microvessel density.