Pericytes in diabetes-associated vascular disease

• Published in: Journal of diabetes and its complications Vol. 30; no. 8; pp. 1643 - 1650
• Main Authors: Warmke, Nele, Griffin, Kathryn J, Cubbon, Richard M
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2016; Elsevier Limited
• Subjects: Angiogenesis; Biology; Cell growth; Diabetes; Diabetes Mellitus - physiopathology; Diabetic Angiopathies - physiopathology; Endocrinology & Metabolism; Endothelial; Endothelial Cells - cytology; Epidermal growth factor; Experiments; Heart attacks; Humans; Microvessels; Pericyte; Pericytes - pathology; Smooth muscle; Vascular; Endothelial; Pericyte; Angiogenesis; Diabetes; Vascular
• ISSN: 1056-8727; 1873-460X
• DOI: 10.1016/j.jdiacomp.2016.08.005

Abstract Pericytes are mural cells that support and stabilise the microvasculature, and are present in all vascular beds. Pericyte-endothelial cell crosstalk is essential in both remodelling and quiescent vasculature, and this complex interaction is often disrupted in disease states. Pericyte loss is believed to be an early hallmark of diabetes-associated microvascular disease, including retinopathy and nephropathy. Here we review the current literature defining pericyte biology in the context of diabetes-associated vascular disease, with a particular focus on whether pericytes contribute actively to disease progression. We also speculate regarding the role of pericytes in the recovery from macrovascular complications, such as critical limb ischaemia. It becomes clear that dysfunctional pericytes are likely to actively induce disease progression by causing vasoconstriction and basement membrane thickening, resulting in tissue ischaemia. Moreover, their altered interactions with endothelial cells are likely to cause abnormal and inadequate neovascularisation in diverse vascular beds. Further research is needed to identify mechanisms by which pericyte function is altered by diabetes, with a view to developing therapeutic approaches that normalise vascular function and remodelling.