Journal
ANNUAL REVIEW OF MEDICINE, VOL 64
Volume 64, Issue -, Pages 357-366Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-med-050311-163340
Keywords
CKD; actin cytoskeleton; dynamin; suPAR; novel therapeutics
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Funding
- NIDDK NIH HHS [R01 DK087985] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK087985] Funding Source: NIH RePORTER
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Proteinuric chronic kidney disease (CKD), once a rare affliction believed to be mainly caused by genetic mutations, has become a global pandemic that severely diminishes the quality of life for millions. Despite the changing face of CKD, treatment options and resources remain woefully antiquated and have failed to arrest or reverse the effects of kidney-related diseases. Histological and genetic data strongly implicate one promising target: the podocyte. Podocytes are terminally differentiated cells of the kidney glomerulus that are essential for the integrity of the kidney filter. Their function is primarily based on their intricate structure, which includes foot processes. Loss of these actin-driven membrane extensions is tightly connected to the presence of protein in the urine, podocyte loss, development of CKD, and ultimately renal failure.
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