Impact of APOL1 kidney risk variants on glomerular transcriptomes

Kidney Int. 2022 Jul;102(1):16-19. doi: 10.1016/j.kint.2022.04.019.

Abstract

McNulty and colleagues describe the glomerular transcriptional landscape of subjects with APOL1 (the gene encoding apolipoprotein L1)-associated kidney disease, using bulk RNA sequencing. They found the following: APOL1 gene expression was higher in individuals with APOL1 high-risk genetic status; in glomeruli, STC1, encoding stanniocalcin, was the most upregulated gene, and CCL18, encoding C-C motif chemokine ligand 18, was the most downregulated gene; and nuclear factor kappa BNF-κB inhibitor-interacting Ras-like 1 (NKIRAS1) is the strongest hub gene. These findings identify disease pathways that might mediate or mitigate APOL1-associated nephropathies.

Publication types

  • Research Support, N.I.H., Intramural
  • Comment

MeSH terms

  • Apolipoprotein L1* / genetics
  • Humans
  • Kidney / metabolism
  • Kidney Diseases* / genetics
  • Kidney Diseases* / metabolism
  • Lipoproteins, HDL / genetics
  • Risk Factors
  • Transcriptome*

Substances

  • APOL1 protein, human
  • Apolipoprotein L1
  • Lipoproteins, HDL