Indoxyl sulfate in uremia: an old idea with updated concepts.
Journal
The Journal of clinical investigation
ISSN: 1558-8238
Titre abrégé: J Clin Invest
Pays: United States
ID NLM: 7802877
Informations de publication
Date de publication:
04 01 2022
04 01 2022
Historique:
entrez:
4
1
2022
pubmed:
5
1
2022
medline:
9
2
2022
Statut:
ppublish
Résumé
Patients with end-stage kidney disease (ESKD) have increased vascular disease. While protein-bound molecules that escape hemodialysis may contribute to uremic toxicity, specific contributing toxins remain ambiguous. In this issue of the JCI, Arinze et al. explore the role of tryptophan metabolites in chronic kidney disease-associated (CKD-associated) peripheral arterial disease. The authors used mouse and zebrafish models to show that circulating indoxyl sulfate (IS) blocked endothelial Wnt signaling, which impaired angiogenesis. Plasma levels of IS and other tryptophan metabolites correlated with adverse peripheral vascular disease events in humans. These findings suggest that lowering IS may benefit individuals with CKD and ESKD.
Identifiants
pubmed: 34981787
pii: 155860
doi: 10.1172/JCI155860
pmc: PMC8718144
doi:
pii:
Substances chimiques
Indican
N187WK1Y1J
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Comment
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL133399
Pays : United States
Commentaires et corrections
Type : CommentOn
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