The podocyte's response to injury: role in proteinuria and glomerulosclerosis - PubMed

Affiliations

• PMID: 16688120
• DOI: 10.1038/sj.ki.5000410

Free article

Review

The podocyte's response to injury: role in proteinuria and glomerulosclerosis

S J Shankland. Kidney Int. 2006 Jun.

Free article

Abstract

The terminally differentiated podocyte, also called glomerular visceral epithelial cell, are highly specialized cells. They function as a critical size and charge barrier to prevent proteinuria. Podocytes are injured in diabetic and non-diabetic renal diseases. The clinical signature of podocyte injury is proteinuria, with or without loss of renal function owing to glomerulosclerosis. There is an exciting and expanding literature showing that hereditary, congenital, or acquired abnormalities in the molecular anatomy of podocytes leads to proteinuria, and at times, glomerulosclerosis. The change in podocyte shape, called effacement, is not simply a passive process following injury, but is owing to a complex interplay of proteins that comprise the molecular anatomy of the different protein domains of podocytes. These will be discussed in this review. Recent studies have also highlighted that a reduction in podocyte number directly causes proteinuria and glomerulosclerosis. This is owing to several factors, including the relative inability for these cells to proliferate, detachment, and apoptosis. The mechanisms of these events are being elucidated, and are discussed in this review. It is the hope that by delineating the events following injury to podocytes, therapies might be developed to reduce the burden of proteinuric renal diseases.

Similar articles

• [The role of podocyte injury in chronic kidney disease].

  Asanuma K. Asanuma K. Nihon Rinsho Meneki Gakkai Kaishi. 2015;38(1):26-36. doi: 10.2177/jsci.38.26. Nihon Rinsho Meneki Gakkai Kaishi. 2015. PMID: 25765686 Review. Japanese.

• Podocyte injury and its consequences.

  Nagata M. Nagata M. Kidney Int. 2016 Jun;89(6):1221-30. doi: 10.1016/j.kint.2016.01.012. Epub 2016 Mar 19. Kidney Int. 2016. PMID: 27165817 Review.

• Regulation of TRPC6 ion channels in podocytes - Implications for focal segmental glomerulosclerosis and acquired forms of proteinuric diseases.

  Szabó T, Ambrus L, Zákány N, Balla G, Bíró T. Szabó T, et al. Acta Physiol Hung. 2015 Sep;102(3):241-51. doi: 10.1556/036.102.2015.3.2. Acta Physiol Hung. 2015. PMID: 26551740 Review.

• Pathogenic role of TGF-β in the progression of podocyte diseases.

  Lee HS. Lee HS. Histol Histopathol. 2011 Jan;26(1):107-16. doi: 10.14670/HH-26.107. Histol Histopathol. 2011. PMID: 21117032 Review.

• Pathogenesis of the podocytopathy and proteinuria in diabetic glomerulopathy.

  Ziyadeh FN, Wolf G. Ziyadeh FN, et al. Curr Diabetes Rev. 2008 Feb;4(1):39-45. doi: 10.2174/157339908783502370. Curr Diabetes Rev. 2008. PMID: 18220694 Review.

Cited by

• Protective effects of peroxisome proliferator-activated receptor agonists on human podocytes: proposed mechanisms of action.

  Miglio G, Rosa AC, Rattazzi L, Grange C, Camussi G, Fantozzi R. Miglio G, et al. Br J Pharmacol. 2012 Oct;167(3):641-53. doi: 10.1111/j.1476-5381.2012.02026.x. Br J Pharmacol. 2012. PMID: 22594945 Free PMC article.

• Conditioned mesenchymal stem cells attenuate progression of chronic kidney disease through inhibition of epithelial-to-mesenchymal transition and immune modulation.

  Chang JW, Tsai HL, Chen CW, Yang HW, Yang AH, Yang LY, Wang PS, Ng YY, Lin TL, Lee OK. Chang JW, et al. J Cell Mol Med. 2012 Dec;16(12):2935-49. doi: 10.1111/j.1582-4934.2012.01610.x. J Cell Mol Med. 2012. PMID: 22862802 Free PMC article.

• Divergent functions of the Rho GTPases Rac1 and Cdc42 in podocyte injury.

  Blattner SM, Hodgin JB, Nishio M, Wylie SA, Saha J, Soofi AA, Vining C, Randolph A, Herbach N, Wanke R, Atkins KB, Gyung Kang H, Henger A, Brakebusch C, Holzman LB, Kretzler M. Blattner SM, et al. Kidney Int. 2013 Nov;84(5):920-30. doi: 10.1038/ki.2013.175. Epub 2013 May 15. Kidney Int. 2013. PMID: 23677246 Free PMC article.

• Vitamin D and its receptor regulate lipopolysaccharide-induced transforming growth factor-β, angiotensinogen expression and podocytes apoptosis through the nuclear factor-κB pathway.

  Xu L, Zhang P, Guan H, Huang Z, He X, Wan X, Xiao H, Li Y. Xu L, et al. J Diabetes Investig. 2016 Sep;7(5):680-8. doi: 10.1111/jdi.12505. Epub 2016 Apr 1. J Diabetes Investig. 2016. PMID: 27180929 Free PMC article.

• Myo1c is an unconventional myosin required for zebrafish glomerular development.

  Arif E, Kumari B, Wagner MC, Zhou W, Holzman LB, Nihalani D. Arif E, et al. Kidney Int. 2013 Dec;84(6):1154-65. doi: 10.1038/ki.2013.201. Epub 2013 May 29. Kidney Int. 2013. PMID: 23715127 Free PMC article.

Publication types

MeSH terms

Substances

LinkOut - more resources

• Full Text Sources

  • Elsevier Science
  • Ovid Technologies, Inc.

• Other Literature Sources

  • The Lens - Patent Citations Database

• Medical

  • MedlinePlus Health Information