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Review
. 2016 May;16(5):45.
doi: 10.1007/s11892-016-0735-5.

Podocytes: the Weakest Link in Diabetic Kidney Disease?

Jamie S Lin  1 , Katalin Susztak  2
Affiliations
Review

Podocytes: the Weakest Link in Diabetic Kidney Disease?

Jamie S Lin et al. Curr Diab Rep. 2016 May.

Abstract

Diabetes is increasing in prevalence and is the leading cause of end-stage renal disease in the United States. Diabetic kidney disease is considered a proteinuric glomerular disease. Although the glomerulus is composed of various cell types, research suggests that podocytes are critical to overall glomerular health. Podocyte injury has been identified as a pivotal event resulting in proteinuric kidney disease, glomerulosclerosis, and loss of renal function. Thus, understanding the signaling mechanisms that trigger podocyte injury in diabetic kidney disease might allow for the development of targeted therapeutics to prevent or ameliorate progression to end-stage renal failure. This review focuses on the role of podocytes in diabetic kidney disease.

Keywords: Albuminuria; Diabetes; Glomerulosclerosis; Notch; Podocytes.

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Figures

Figure 1
Figure 1
A. Tripartite glomerular filtration barrier includes fenestrated glomerular endothelial cells, glomerular basement membrane, and podocytes. Foot processes interdigitate with neighboring podocyte foot processes creating slit diaphragms. B. Diabetic kidney disease results in glomerular basement membrane thickening and injury to the podocytes depicted by foot process effacement, detachment, and disruption of the slit diaphragm resulting in albumin leakage across the glomerular filtration barrier. C. Podocyte loss results in hypertrophy and/or dedifferentiation, increase albuminuria, and functional kidney decline.
Figure 1
Figure 1
A. Tripartite glomerular filtration barrier includes fenestrated glomerular endothelial cells, glomerular basement membrane, and podocytes. Foot processes interdigitate with neighboring podocyte foot processes creating slit diaphragms. B. Diabetic kidney disease results in glomerular basement membrane thickening and injury to the podocytes depicted by foot process effacement, detachment, and disruption of the slit diaphragm resulting in albumin leakage across the glomerular filtration barrier. C. Podocyte loss results in hypertrophy and/or dedifferentiation, increase albuminuria, and functional kidney decline.
Figure 1
Figure 1
A. Tripartite glomerular filtration barrier includes fenestrated glomerular endothelial cells, glomerular basement membrane, and podocytes. Foot processes interdigitate with neighboring podocyte foot processes creating slit diaphragms. B. Diabetic kidney disease results in glomerular basement membrane thickening and injury to the podocytes depicted by foot process effacement, detachment, and disruption of the slit diaphragm resulting in albumin leakage across the glomerular filtration barrier. C. Podocyte loss results in hypertrophy and/or dedifferentiation, increase albuminuria, and functional kidney decline.
Figure 2
Figure 2
Various complex inter- and intracellular signaling mechanisms have been described in diabetes-induced podocyte injury.
See this image and copyright information in PMC

References

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