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Evaluation of Zebrafish Kidney Function Using a Fluorescent Clearance Assay
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APOL1 and kidney cell function.

Vinod Kumar1, Pravin C Singhal1

  • 1Institute of Molecular Medicine, Feinstein Institute for Medical Research and Department of Medicine, Zucker School of Medicine at Hofstra-Northwell, Hempstead, New York.

American Journal of Physiology. Renal Physiology
|June 27, 2019
PubMed
Summary
This summary is machine-generated.

Apolipoprotein L1 (APOL1) risk variants are linked to chronic kidney diseases (CKDs). This review explores whether a loss of APOL1 non-risk function, rather than a gain of risk function, contributes to APOL1-associated CKDs.

Keywords:
apolipoprotein L1chronic kidney diseasefocal segmental glomerulosclerosishuman immunodeficiency virus-associated nephropathypodocyte

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Area of Science:

  • Genetics
  • Nephrology
  • Cell Biology

Background:

  • The apolipoprotein L1 (APOL1) gene, unique to humans and gorillas, has variants (APOL1 RRVs) associated with higher rates of chronic kidney diseases (CKDs) in individuals of African ancestry.
  • While APOL1 RRVs induce cytotoxicity in cell models, elevated levels are not observed in patients with APOL1-associated CKDs, questioning the mechanism of kidney injury.

Purpose of the Study:

  • To analyze the literature on the function of APOL1 non-risk variants (G0).
  • To investigate how the loss of APOL1 non-risk functions may contribute to APOL1-associated CKDs.

Main Methods:

  • Literature review of existing studies on APOL1 gene function and its role in kidney disease.
  • Analysis of cellular mechanisms, including cytotoxicity, gene expression, and molecular pathways related to APOL1 variants.

Main Results:

  • APOL1 RRVs induce various forms of cell death (necrosis, apoptosis, pyroptosis) in cell types like podocytes.
  • Mechanisms of toxicity involve lysosomal swelling, mitochondrial dysfunction, and endoplasmic reticulum stress in a dose-dependent manner.
  • Crucially, cellular and circulating levels of APOL1 RRVs are not elevated in CKD patients, challenging a simple gain-of-function hypothesis.

Conclusions:

  • The pathogenic mechanism of APOL1 RRVs in CKDs remains unclear, with evidence suggesting a potential loss-of-function of APOL1 non-risk variants.
  • Understanding the normal functions of APOL1 non-risk variants is critical for elucidating their role in kidney disease pathogenesis.