antiangiogenese

Antiangiogenesis, also spelled anti-angiogenesis, refers to strategies that inhibit the growth of new blood vessels, a process known as angiogenesis. In medicine, antiangiogenic therapy aims to deprive tumors or other pathological tissues of their blood supply, thereby slowing growth or triggering regression. The approach targets pro-angiogenic signals and endothelial cell function to disrupt neovascularization.

The dominant target is the vascular endothelial growth factor (VEGF) pathway. Therapeutic approaches include monoclonal antibodies against VEGF (for example, bevacizumab), soluble decoy receptors (aflibercept), and small-molecule receptor tyrosine kinase inhibitors (RTKIs) that block VEGF receptors and related signaling pathways. Other strategies address angiopoietins/TIE2, fibroblast growth factor, platelet-derived growth factor, and integrins, among others. Antiangiogenic agents can act by inhibiting endothelial cell proliferation, normalizing abnormal tumor vasculature, or enhancing the effectiveness of other therapies.

Clinical use spans oncology and ophthalmology. In cancer, antiangiogenic drugs can slow tumor growth, reduce metastasis, and improve the delivery of chemotherapy or immunotherapy. In eye diseases such as age-related macular degeneration and proliferative diabetic retinopathy, intravitreal VEGF inhibitors reduce neovascularization and edema, preserving vision in many cases.

Limitations and risks include innate or acquired resistance, where tumors adapt by upregulating alternative pro-angiogenic pathways or exploiting existing vessels. Adverse effects may involve hypertension, thromboembolism, wound-healing impairment, proteinuria, and hemorrhage. Ocular therapy carries risks of infection and inflammation. The field continues to refine targets and combinations to improve efficacy and safety.