What is it about?

This paper provides a molecular and cellular explanation for kidney disease due to the expression of APOL1 variants that protect humans against sleeping sickness. The aim of this paper is to summarize and explain to a medical audience, the data recently published by my laboratory in a molecular biology journal (Cell Reports March 2020).

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Why is it important?

This is the first detailed explanation for the mechanism of kidney disease due to APOL1 variants. It also highlights the importance of the phosphoinositide PI4P for the biology of kidney podocytes.

Perspectives

This opens new perspectives for the treatment or prevention of kidney disease due to APOL1 variants.

Etienne Pays
Universite Libre de Bruxelles Bibliotheque des Sciences Humaines

The podocyte dysfunctions observed upon APOL3 inactivation by APOL1 variants help to understand the role of APOLs in cellular biology, particularly their role in the control of mitochondrion fission or fusion. As this role applies to all cell types, APOL1 variants should affect cellular physiology in general.

Etienne Pays
Universite Libre de Bruxelles Bibliotheque des Sciences Humaines

Read the Original

This page is a summary of: The Mechanism of Kidney Disease Due to APOL1 Risk Variants, Journal of the American Society of Nephrology, September 2020, American Society of Nephrology, DOI: 10.1681/asn.2020070954.
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