ArticleRenal failure2024
Usp9x contributes to the development of sepsis-induced acute kidney injury by promoting inflammation and apoptosis in renal tubular epithelial cells via activation of the TLR4/nf-κb pathway.
Article in Renal failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Pioglitazone Attenuates Sepsis-Associated Acute Kidney Injury by Modulating TLR-4/NF-κB Signaling and Improving Survival and Renal Function.Journal of clinical medicine · 2026Article
- The Role of Ubiquitination and Deubiquitination in the Pathogenesis of Acute Kidney Injury: Progress in Research.Biomedicines · 2025Review
- USP18 promotes ferroptosis in lipopolysaccharide-induced human kidney organoids by stabilizing STING1.Cell biology and toxicology · 2025Article
- β‑elemene attenuates IRI‑AKI by inhibiting inflammation and apoptosis via suppression of the TLR4/MyD88/NF‑κB/MAPK signal axis activation.Molecular medicine reports · 2025Article
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Prognostic value of blood urea nitrogen to albumin ratio in septic patients with acute kidney injury-a retrospective study based on MIMIC database.Frontiers in medicine · 2025Article
- The roles of the ubiquitin-proteasome system in renal disease.International journal of medical sciences · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a pattern recognition receptor, Toll-like receptor 4 (TLR4) is crucial for the development and progression of acute kidney injury (AKI). This study aims to explore whether the deubiquitinase Usp9x influences the TLR4/NF-B pathway to cause sepsis-induced acute kidney injury (S-AKI). The model of AKI was established in Sprague-Dawley rats using the cecal ligation and puncture (CLP) method, while renal tubular epithelial cell NRK-52E was stimulated with lipopolysaccharide (LPS)
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Registered trials
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