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Podocytes: the Weakest Link in Diabetic Kidney Disease?

  • Microvascular Complications—Nephropathy (AP Maxwell, Section Editor)
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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.

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Authors and Affiliations

  1. Renal-Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA

    Jamie S. Lin & Katalin Susztak

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  1. Jamie S. Lin
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  2. Katalin Susztak
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Correspondence to Katalin Susztak.

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Conflict of Interest

Jamie S. Lin declares that she has no conflict of interest. Katalin Susztak reports that work in her lab is supported by Biogen, Boehringer Ingelheim, and Lilly.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Funding

Work in the Susztak lab is supported by the National Institute of Health, Juvenile Diabetes Research Foundation, American Diabetes Association, Boehringer Ingelheim, Biogen, and Lilly. Dr. Lin is supported by NIDDK Ruth L. Kirschstein National Research Service Award institutional research training and post-doctoral fellowship grant.

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This article is part of the Topical Collection on Microvascular Complications—Nephropathy

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Lin, J.S., Susztak, K. Podocytes: the Weakest Link in Diabetic Kidney Disease?. Curr Diab Rep 16, 45 (2016). https://doi.org/10.1007/s11892-016-0735-5

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