Pericytes are distinctive regulators of angiogenesis and are adumbrated to provide vessel stability and control of endothelial proliferation. The present article spotlights the persona of pericytes in physiological angiogenesis, recruitment of pericytes and different mechanisms of pericyte depletion. Developing retina appears particularly dependent on pericytes, and pericyte loss is considered as hallmark of early diabetic retinopathies. Several factors are contemplated to be engaged in pericyte conscription including angiopoietin-1 and its receptor tyrosine kinase Tie-2, vascular endothelial growth factor-A and its receptor flk-1 and the platelet-derived growth factor PDGF-B/PDGF-beta system. At present, the mechanisms by which diabetes persuade apoptosis in the retinal microvasculature remain indecisive, albeit oxidative stress, formation of advanced glycation end products , upregulation of protein kinase C, increased polyol pathway flux and focal leukostasis may be important. In this context, accelerated microvascular cell death may become a constructive surrogate end-point in pharmacological studies of experimental diabetic.