ArticleInternational urology and nephrology2023
miR-22 alleviates sepsis-induced acute kidney injury via targeting the HMGB1/TLR4/NF-κB signaling pathway.
Article in International urology and nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Expression of MicroRNAs in Sepsis-Related Organ Dysfunction: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Review
- 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
- Curcumin Alleviates Sepsis-Associated Acute Kidney Injury Potentially by Inhibiting Ferroptosis Through the ACSL4/GPX4 Signaling Pathway.Drug development research · 2025Article
- Exosomes and microRNA - a new form of remote and bidirectional neuroimmunomodulation?Neuroimmunomodulation · 2025Review
- Unveiling the Therapeutic Potential of Dulaglutide in Mitigating Tacrolimus-Induced Nephrotoxicity Through Targeting the miR-22/HMGB-1/TLR4/MyD88/NF-κB Trajectory.Archiv der Pharmazie · 2025Article
- Clinical significance of miR-625-5p in patients with sepsis-induced acute kidney injury based on bioinformatics analysis.International urology and nephrology · 2025Article
- High-mobility group box 1 in acute kidney injury.Frontiers in pharmacology · 2025Review
- Article
- miR-16-5p aggravates sepsis-associated acute kidney injury by inducing apoptosis.Renal failure · 2024Article
- Review
- High-mobility group box 1 and its related receptors: potential therapeutic targets for contrast-induced acute kidney injury.International urology and nephrology · 2024Review
- Knockdown of circ-Gatad1 alleviates LPS induced HK2 cell injury via targeting miR-22-3p/TRPM7 axis in septic acute kidney.BMC nephrology · 2024Article
- PTEN in kidney diseases: a potential therapeutic target in preventing AKI-to-CKD transition.Frontiers in medicine · 2024Review
- MicroRNAs as Biomarkers and Therapeutic Targets for Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute kidney injury (AKI) is a severe complication of sepsis, and is strongly correlated with MicroRNAs (miRNAs). However, the mechanism of miR-22 on sepsis-induced AKI is not clearly understood. The study aimed to explore the role and mechanism of miR-22 on AKI.
methodsThe AKI models were established by cecal ligation and puncture (CLP) surgery in SD rats and lipopolysaccharide (LPS) induction in HBZY-1 cells. In AKI rats, the content of serum creatinine (SCr) and blood urea nitrogen (BUN) were detected. Kidney tissues were pathologically examined by H&E and PAS staining. The LPS-induced HBZY-1 cells were transfected with mimics miR-22, si-HMGB1, or oe-HMGB1. miR-22 and HMGB1 expression was detected in vivo and in vitro. In transfected cells, HMGB1/TLR4/NF-κB pathway-related protein expressions were measured by Western blot. The relationship between miR-22 and HMGB1 was assessed by a dual-luciferase gene report. Inflammatory cytokine levels in serum and cells were assessed by ELISA.
resultsIn AKI rats, kidney injury was observed, accompanied by the down-regulated miR-122 expression and up-regulated HMBG1 expression. The dual-luciferase report found miR-22-3p could targetly regulate HMBG1. Furthermore, both in vitro and in vivo experiments revealed that the releases of inflammatory cytokine were increased after AKI modeling, but the situation was reversed by mimics miR-22 or si-HMGB1 in vitro. In HBZY-1 cells, mimics miR-22 could suppress LPS-induced overexpression of HMGB1/TLR4/NF-κB signaling pathway-related proteins. However, the oe-HMGB1 addition reversed the effect of mimics miR-22.
conclusionmiR-22 can inhibit the inflammatory response, target the HMGB1, and inhibit the HMGB1/TLR4/NF-kB pathway, to attenuate the sepsis-induced AKI, which indicates that miR-22 may serve as a potential treatment target in sepsis-induced AKI.
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