ArticleJournal of bioenergetics and biomembranes2023
Circ_0001714 knockdown alleviates lipopolysaccharide-induced apoptosis and inflammation in renal tubular epithelial cells via miR-129-5p/TRAF6 axis in septic acute kidney injury.
Article in Journal of bioenergetics and biomembranes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Predicting acute kidney injury in children with sepsis using red blood cell distribution and biomarkers (PCT, IL-6, CRP, and cystatin C).Journal of medical biochemistry · 2025Article
- Embryonic Lethal Abnormal Visual-Like Protein 1 Aggravates Caerulein-Induced AR42J Cell Injury and Macrophage M1 Polarization to Accelerate Acute Pancreatitis by Upregulating TRAF6.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2025Article
- Astragaloside IV relieves passive heymann nephritis and podocyte injury by suppressing the TRAF6/NF-κb axis.Renal failure · 2024Article
- Discovery and verification of mmu_Circ_26986/hsa_Circ_0072463 as a potential biomarker and intervention target for sepsis-associated acute kidney injury.Cellular and molecular life sciences : CMLS · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCircular RNAs (circRNAs) have been shown to play roles in regulating sepsis. Sepsis is a major cause of acute kidney injury (AKI). Herein, we aimed to investigate the role and mechanism of circ_0001714 in the progression of sepsis-induced AKI.
methodsHuman HK-2 cells were exposed to lipopolysaccharide (LPS) for functional experiments. Quantitative real-time polymerase chain reaction and western blotting were used for expression analysis. Functional experiments were performed by using MTT assay, 5-ethynyl-2'-deoxyuridine assay, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). The binding between miR-129-5p and circ_0001714 or TRAF6 (TNF receptor associated factor 6) was validated using dual-luciferase reporter assay.
resultsCirc_0001714 expression was higher in sepsis-AKI patients. HK-2 cells were exposed to LPS to imitate the injury of renal tubular epithelial cells during sepsis-AKI. LPS dose-dependently up-regulated circ_0001714, moreover, circ_0001714 silencing reversed LPS-evoked apoptosis and inflammation in HK-2 cells. Mechanistically, circ_0001714 sequestered miR-129-5p to up-regulate TRAF6 expression, implying the circ_0001714/miR-129-5p/TRAF6 feedback loop. MiR-129-5p was decreased, while TRAF6 was increased in sepsis-AKI patients and LPS-stimulated HK-2 cells. MiR-129-5p re-expression or TRAF6 silencing protected against LPS-induced HK-2 cell apoptosis and inflammation. Additionally, a series of rescue experiments showed that miR-129-5p inhibition reversed the inhibitory action of circ_0001714 knockdown on LPS-induced HK-2 cell injury. Furthermore, TRAF6 overexpression also attenuated the protective effects of miR-129-5p on HK-2 cells under LPS treatment.
conclusionCirc_0001714 silencing might alleviate LPS-induced apoptosis and inflammation via targeting miR-129-5p/TRAF6 axis in HK-2 cells.
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