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Pathologic angiogenesis takes place in numerous diseases such as cancer, diabetic retinopathy, agerelated macula degeneration, retinal vein occlusion, the aids dementia complex, rheumatoid arthritis, psoriasis, inflammatory bowel diseases, endometriosis and many more.The neovascularization is regarded to be causative for the detrimental effects of some diseases and to take part in the progression of others.Common characteristics of pathological neovascularization include abnormal Acalabrutinib vascular permeability and defective vascular remodeling and maturation, which promote leakage, hemorrhaging and inflammation.Pericytes and vascular smooth muscle cells reside at the interface between the endothelium and the surrounding tissue and are as such ideally positioned to take an active part in the angiogenic process. Several functions of pericytes relevant to angiogenesis have been proposed.Pericytes may sense the hemodynamic forces within the vessel, act in paracrine and cellcell contactdependent control of endothelial proliferation and differentiation, and contact numerous endothelial cells and thus integrate the signals along the vessel length.In some diseases, such as diabetic retinopathy, it is speculated that pericytes are the primarily affected vascular cells, leading to secondary changes of the endothelium, and to dysregulated angiogenesis.In the diseases mentioned, inhibition of pathological neovascularization is a therapeutic goal.Accumulating data now point to pericytes as a potential antiangiogenic Hematoxylin target complementary to the endothelium. Conversely, stimulation of neovascularization may be favorable in ischemic diseases of the limbs and the heart.The need to stabilize newly formed vessels after successful induction of neovascularization places pericytes in focus also in proangiogenic therapies. However, our understanding of pericytes is still limited compared to that of the endothelial cells.For a deeper understanding of angiogenesis and how it can be modulated in therapeutic situations, it is important to further decipher the mechanisms controlling pericyte smooth muscle cell recruitment and function.The present review focuses on the mechanisms of pericyte recruitment in developmental angiogenesis and the lessons learnt about the functions of pericytes from genetic states of pericyte deficiency.The arteries and veins are surrounded by single or multiple layers of vSMC, whereas the smallest capillaries are partially covered by solitary cells referred to as pericytes.Intermediatesize vessels, arterioles and venules, have mural cells with properties intermediate between those of typical vSMC and pericytes.Based on the morphological similarities and the expression of some common marker genes like asmooth muscle actin and desmin, it has been suggested that vSMC and pericytes represent phenotypic variants of a continuous population of mural cells, sharing the same lineage.The phenotypic variation would reflect different subspecialization in accordance with the location in the vascular system. Depending on external stimuli, pericytes have been suggested to give rise to vSMC and vice versa. Thus, pericytes may function as progenitors for vSMC in cases of vessel enlargement or remodeling. In wound healing and inflammatory processes it has been suggested that pericytes detach from the vessel wall and differentiate into a collagen typeI producing, fibroblastlike cell. Thus, pericytes may contribute to the formation of the fibrotic components of scars, to other situations of inflammationassociated tissue fibrosis, and to fibrous tumor stroma formation.They are not in direct cellcell contact with the endothelial cells but are separated from the endothelium by a basement membrane, and in larger arteries by a tissue layer called the intima.

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