Angiogenesis refers to the process through which new blood vessels form from pre-existing ones. This mechanism involves the sprouting and growth of endothelial cells. New capillaries develop to deliver oxygen and nutrients to tissues and remove waste products. This process is carefully regulated by a balance of various molecular signals, ensuring blood vessel formation occurs only when and where it is needed.
Angiogenesis in Normal Body Functions
Angiogenesis plays a role in many normal bodily functions, starting even before birth. During embryonic development, new blood vessels form to deliver oxygen and nutrients to developing tissues and organs. This initial network is crucial for the growth and differentiation of cells throughout the embryo.
Angiogenesis is a continuous process throughout life, adapting to the metabolic demands of various tissues. It is particularly active in wound healing, where new blood vessels form to restore blood supply to damaged areas, providing the necessary oxygen and nutrients for tissue repair.
The female reproductive system is another example where angiogenesis occurs as a regular, cyclical process. The uterine lining, or endometrium, undergoes significant blood vessel growth to prepare for a potential pregnancy each menstrual cycle. If conception occurs, angiogenesis ensures adequate blood flow to the placenta, supporting fetal development and growth.
Angiogenesis in Disease Development
While normally beneficial, uncontrolled angiogenesis can contribute to various diseases. A primary example is cancer, where tumors hijack the angiogenic process to support their rapid growth and spread. Tumors release specific growth factors, such as vascular endothelial growth factor (VEGF), which stimulate the formation of new blood vessels that supply the tumor with oxygen and nutrients.
These tumor blood vessels are often abnormal, being dilated, irregularly shaped, and leaky. This pathological angiogenesis not only fuels tumor growth but also facilitates metastasis, as the leaky vessels provide an easier pathway for cells to enter the bloodstream.
Beyond cancer, pathological angiogenesis contributes to other conditions, such as age-related macular degeneration (AMD). In the “wet” form of AMD, abnormal, leaky blood vessels grow beneath the macula, the central part of the retina. These vessels can leak fluid and blood, damaging the delicate nerves responsible for central vision and potentially leading to scarring and permanent vision loss. Inflammatory conditions like rheumatoid arthritis also involve excessive angiogenesis, where new blood vessels contribute to the inflammation and destruction of joint tissues.
Modulating Angiogenesis for Health
Understanding angiogenesis has opened avenues for therapies. One approach involves promoting angiogenesis, beneficial in conditions where blood supply is insufficient. For instance, in ischemic heart disease or peripheral vascular diseases, therapies aim to stimulate new blood vessel formation to restore circulation and improve tissue perfusion. This can involve delivering pro-angiogenic factors like vascular endothelial growth factor (VEGF) or hepatocyte growth factor (HGF) to the affected areas. In wound healing, enhancing angiogenesis can accelerate the repair of chronic wounds and burns by increasing blood supply to the injured site.
Conversely, inhibiting angiogenesis is a strategy employed to treat diseases characterized by excessive blood vessel growth. Anti-angiogenic drugs are widely used in cancer treatment to starve tumors by blocking the formation of new blood vessels, thereby limiting their access to nutrients and oxygen. These drugs often target VEGF or its receptors, preventing the signaling that drives new vessel formation. Similarly, in wet age-related macular degeneration, anti-VEGF agents are injected into the eye to reduce the growth and leakage from abnormal blood vessels, helping to preserve vision. The concept of an “angiogenic switch” describes the shift in balance between pro-angiogenic and anti-angiogenic factors that can trigger or suppress new vessel formation, guiding these therapeutic strategies.