الفهرس 
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Abstract
Angiogenesis is the physiological process through which new blood vessels form from pre-existing vessels. This is distinct from vasculogenesis, which is the de novo formation of endothelial cells from mesoderm cell precursors. The first vessels in the developing embryo form through vasculogenesis, after which angiogenesis is responsible for most, if not all, blood vessel growth during development and in disease. Angiogenesis may be a target for combating diseases characterized by either poor vascularisation or abnormal vasculature. Application of specific compounds that may inhibit or induce the creation of new blood vessels in the body may help combat such diseases. The presence of blood vessels where there should be none may affect the mechanical properties of a tissue, increasing the likelihood of failure. Excess angiogenesis underlies many disease processes in dermatology, from those that seem obvious (neoplastic disease), but also ulceration, in which excess angiogenesis prevents reepithelialization, to inflammatory processes (psoriasis, atopic dermatitis, lupus), and even chronic infections like leprosy.
Excessive angiogenesis has also been implicated in the pathogenesis of several malignant, pre-malignant, and non-malignant skin conditions. Indeed, skin cancers also require a blood supply to grow larger than a few millimeters in diameter, while pre-cancerous skin lesions and warts have a higher density of capillaries when compared to surrounding normal skin.
Furthermore, excessive exposure to ultraviolet (UV) radiation - an important risk factor for many skin lesions – triggers angiogenesis in the skin by increasing levels of stimulators such as VEGF and b-FGF while suppressing angiogenesis inhibitors. Of note, the progression from pre-cancerous skin lesions to overt skin cancer is accompanied by the continued growth of new blood vessels.
Like all solid malignancies, cancers occurring in skin are highly angiogenic. Vascular tumors of the skin, such as Kaposi’s sarcoma, hemangioma of infancy, pyogenic granuloma, and angiosarcoma, are composed of proliferating cells of endothelial origin and are also angiogenesis-dependent. Anti-angiogenic agents have been approved by the US Food and Drug Administration: bevacizumab and ziv-aflibercept as antivascular endothelial growth factor (VEGF) agents, whereas sorafenib, sunitinib, pazopanib, axitinib, cabozantinib and regorafenib are approved as small-molecule RTK (receptor tyrosine kinase) inhibitors.