APOL1 variant associated kidney disease: From trypanosomes to podocyte cytoskeleton.

Expression of the C-terminal APOL1 variants G1 and G2 is strongly linked to chronic kidney disease. The recent analysis of podocytes genetically engineered to express either C-terminal truncated APOL1 or disrupted APOL3 allowed the conclusion that C-terminal APOL1 variants induce reorganization of actomyosin activities through inhibition of APOL3 functions. This editorial is not intended to review the literature in the field, but rather to discuss the proposal that podocyte dysfunctions linked to APOL3 inactivation can account for chronic kidney disease linked to expression of the APOL1 risk variants G1 and G2.
Source: Kidney International - Category: Urology & Nephrology Authors: Tags: editorial Source Type: research