STAT1 aggravates kidney injury by NOD-like receptor (NLRP3) signaling in MRL-lpr mice.
Lupus nephritis
NOD-like signaling pathway
STAT1
Journal
Journal of molecular histology
ISSN: 1567-2387
Titre abrégé: J Mol Histol
Pays: Netherlands
ID NLM: 101193653
Informations de publication
Date de publication:
10 Jun 2024
10 Jun 2024
Historique:
received:
24
09
2023
accepted:
27
05
2024
medline:
10
6
2024
pubmed:
10
6
2024
entrez:
10
6
2024
Statut:
aheadofprint
Résumé
Systemic lupus erythematosus (SLE) is a persistent autoimmune disorder that can culminate in lupus nephritis (LN), an intricate renal complication. In pursuit of unraveling the intricate molecular underpinnings governing LN progression, we conducted bioinformatics analysis employing gene expression data sourced from the GSE32591 dataset. Our scrutiny revealed a panoply of differentially expressed genes (DEGs) within the glomerulus and tubulointerstitial compartments of LN patients. Enrichment analysis for DEGs engaged in diverse processes, encompassing virus defense, viral life cycle, cell adhesion molecules, and the NOD-like receptor signaling pathway. Notably, STAT1 emerged as an eminent central hub gene intrinsically tied to NOD-like receptor signaling. To explore the functional significance of STAT1 in the context of LN, MRL-lpr mice model was used to knockout STAT1. The results unveiled that STAT1 silencing yielded a migratory effect on kidney injury, concurrently curbing inflammatory markers. Meanwhile, knockout STAT1 also reduced NLRP3 expression and Cleaved caspase-1 expression. These findings offer tantalizing prospects for targeting STAT1 as a potential therapeutic conduit in the management of LN.
Identifiants
pubmed: 38856930
doi: 10.1007/s10735-024-10208-2
pii: 10.1007/s10735-024-10208-2
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : 2022 Anhui Medical University Scientific Research Fund Project
ID : 2022xkj238
Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer Nature B.V.
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