Angiogenesis is the process by which new blood vessels form from existing ones. It is essential in normal physiology, for example during embryonic development, wound healing and the menstrual cycle, but also plays a major role in diseases such as cancer, diabetic eye disease and rheumatoid arthritis.

The process is tightly controlled by a balance between pro angiogenic and anti angiogenic factors. Key stimulators include vascular endothelial growth factor (VEGF), fibroblast growth factors and angiopoietins, which are released in response to low oxygen or tissue injury. These signals activate endothelial cells lining blood vessels, causing them to proliferate, degrade surrounding matrix, migrate and organize into new capillary tubes. Pericytes and smooth muscle cells then stabilize the nascent vessels. Inhibitors such as thrombospondin, endostatin and angiostatin keep this growth in check. Pathology occurs when this balance is disturbed.

In cancer, tumors often upregulate VEGF and related factors to build their own blood supply, enabling growth and metastasis. This understanding led to anti angiogenic therapies that block VEGF signaling or other components of the vascular growth pathway. These drugs can starve tumors of oxygen and nutrients and are now used in multiple cancers, though resistance and side effects remain challenges.

Conversely, in ischemic heart disease and peripheral artery disease insufficient blood vessel growth contributes to tissue damage. Here, pro angiogenic strategies including growth factor delivery, gene therapy and cell based approaches aim to restore blood flow. Ongoing research focuses on understanding the cellular and molecular mechanisms of angiogenesis, improving the specificity and durability of therapies and identifying biomarkers that predict treatment response.