Impact of APOL1 kidney risk variants on glomerular transcriptomes.


Journal

Kidney international
ISSN: 1523-1755
Titre abrégé: Kidney Int
Pays: United States
ID NLM: 0323470

Informations de publication

Date de publication:
07 2022
Historique:
received: 29 12 2021
revised: 20 04 2022
accepted: 27 04 2022
entrez: 23 6 2022
pubmed: 24 6 2022
medline: 28 6 2022
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 35738828
pii: S0085-2538(22)00365-9
doi: 10.1016/j.kint.2022.04.019
pii:
doi:

Substances chimiques

APOL1 protein, human 0
Apolipoprotein L1 0
Lipoproteins, HDL 0

Types de publication

Journal Article Research Support, N.I.H., Intramural Comment

Langues

eng

Sous-ensembles de citation

IM

Pagination

16-19

Commentaires et corrections

Type : CommentOn

Informations de copyright

Published by Elsevier Inc.

Auteurs

Jeffrey B Kopp (JB)

National Institutes of Health, Bethesda, Maryland, USA. Electronic address: jbkopp@nih.gov.

Jurgen Heymann (J)

National Institutes of Health, Bethesda, Maryland, USA.

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Classifications MeSH