ArticleJournal of molecular histology2024
STAT1 aggravates kidney injury by NOD-like receptor (NLRP3) signaling in MRL-lpr mice.
Article in Journal of molecular histology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Integrative Analyses Identify a cGAS-STING Pathway-Driven Signature With Context-Dependent Roles in Systemic Lupus Erythematosus.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Structural dynamics, pathogenic mechanisms, and therapeutic targeting of the NLRP3 inflammasome in lupus nephritis.Frontiers in immunology · 2026Review
- Hyperoside Attenuates Lupus Nephritis-Associated Mesangial Cell Apoptosis via the P53/XAF1 Pathway: Integrative Bioinformatics and In Vitro Validation.Journal of inflammation research · 2026Article
- Jiawei fangji huangqi decoction inhibits renal fibrosis and inflammation in UUO-induced fibrotic kidneys.Renal failure · 2025Article
- Identification of Shared Biomarkers in Chronic Kidney Disease and Diabetic Nephropathy Using Single-Cell Sequencing.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.