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Impact of APOL1 kidney risk variants on glomerular transcriptomes.

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.
AuthorsJeffrey B Kopp, Jurgen Heymann
JournalKidney international (Kidney Int) Vol. 102 Issue 1 Pg. 16-19 (07 2022) ISSN: 1523-1755 [Electronic] United States
PMID35738828 (Publication Type: Journal Article, Research Support, N.I.H., Intramural, Comment)
CopyrightPublished by Elsevier Inc.
Chemical References
  • APOL1 protein, human
  • Apolipoprotein L1
  • Lipoproteins, HDL
Topics
  • Apolipoprotein L1 (genetics)
  • Humans
  • Kidney (metabolism)
  • Kidney Diseases (genetics, metabolism)
  • Lipoproteins, HDL (genetics)
  • Risk Factors
  • Transcriptome

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