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Microvascular pericytes in healthy and diseased kidneys

Authors Pan S, Chang Y, Lin S

Received 21 October 2013

Accepted for publication 22 November 2013

Published 17 January 2014 Volume 2014:7 Pages 39—48

DOI https://doi.org/10.2147/IJNRD.S37892

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3


Szu-Yu Pan,1,2 Yu-Ting Chang,3 Shuei-Liong Lin1,3

1Renal Division, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan; 2Department of Internal Medicine, National Taiwan University Hospital, Yun-Lin Branch, Yun-Lin, Taiwan; 3Graduate Institute of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan

Abstract: Pericytes are interstitial mesenchymal cells found in many major organs. In the kidney, microvascular pericytes are defined anatomically as extensively branched, collagen-producing cells in close contact with endothelial cells. Although many molecular markers have been proposed, none of them can identify the pericytes with satisfactory specificity or sensitivity. The roles of microvascular pericytes in kidneys were poorly understood in the past. Recently, by using genetic lineage tracing to label collagen-producing cells or mesenchymal cells, the elusive characteristics of the pericytes have been illuminated. The purpose of this article is to review recent advances in the understanding of microvascular pericytes in the kidneys. In healthy kidney, the pericytes are found to take part in the maintenance of microvascular stability. Detachment of the pericytes from the microvasculature and loss of the close contact with endothelial cells have been observed during renal insult. Renal microvascular pericytes have been shown to be the major source of scar-forming myofibroblasts in fibrogenic kidney disease. Targeting the crosstalk between pericytes and neighboring endothelial cells or tubular epithelial cells may inhibit the pericyte-myofibroblast transition, prevent peritubular capillary rarefaction, and attenuate renal fibrosis. In addition, renal pericytes deserve attention for their potential to produce erythropoietin in healthy kidneys as pericytes stand in the front line, sensing the change of oxygenation and hemoglobin concentration. Further delineation of the mechanisms underlying the reduced erythropoietin production occurring during pericyte-myofibroblast transition may be promising for the development of new treatment strategies for anemia in chronic kidney disease.

Keywords: endothelial cell, fibroblast, chronic kidney disease, myofibroblast, renal fibrosis

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