ArticleInflammation2019
MiR-590-3p Attenuates Acute Kidney Injury by Inhibiting Tumor Necrosis Factor Receptor-Associated Factor 6 in Septic Mice.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- MicroRNA (miR)-590-3p alleviates high-glucose induced renal tubular epithelial cell damage by targeting C-X3-C motif chemokine ligand 1 (CX3CL1) in diabetic nephropathy.Bioengineered · 2022Trial
- The TRAF6-TXNIP-NLRP3 signaling axis regulates LPS-induced pyroptosis in glomerular podocytes.Journal of molecular histology · 2026Article
- Integrated bioinformatics analysis unravels mitochondrial-immune crosstalk and infiltration dynamics in sepsis progression.European journal of medical research · 2025Article
- Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025Review
- Astragaloside IV relieves passive heymann nephritis and podocyte injury by suppressing the TRAF6/NF-κb axis.Renal failure · 2024Article
- Predictive value of miR-582-5p for onset of sepsis-induced acute kidney injury and its functional role during disease development.Central-European journal of immunology · 2024Article
- MicroRNAs as Biomarkers and Therapeutic Targets for Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2023Review
- miR-22 alleviates sepsis-induced acute kidney injury via targeting the HMGB1/TLR4/NF-κB signaling pathway.International urology and nephrology · 2023Article
- MicroRNAs in septic acute kidney injury.Burns & trauma · 2023Article
- MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022Review
- Extracellular vesicles derived from patients with antibody-mediated rejection induce tubular senescence and endothelial to mesenchymal transition in renal cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- miR-30a-5p promotes glomerular podocyte apoptosis via DNMT1-mediated hypermethylation under hyperhomocysteinemia.Acta biochimica et biophysica Sinica · 2022Article
- MicroRNA miR-24-3p Mediates the Negative Regulation of Lipopolysaccharide-Induced Endometrial Inflammatory Response by Targeting TNF Receptor-Associated Factor 6 (Journal of inflammation research · 2022Article
- Non-Coding RNAs in Sepsis-Associated Acute Kidney Injury.Frontiers in physiology · 2022Review
- Downregulation of miR-29b-3p aggravates podocyte injury by targeting HDAC4 in LPS-induced acute kidney injury.The Kaohsiung journal of medical sciences · 2021Article
- Pathogenesis and Treatment of Cytokine Storm Induced by Infectious Diseases.International journal of molecular sciences · 2021Review
- LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p.Experimental and therapeutic medicine · 2020Article
- Bioinformatics-Based Study to Investigate Potential Differentially Expressed Genes and miRNAs in Pediatric Sepsis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses.Inflammation · 2020Article
- MicroRNA-145-5p attenuates high glucose-induced apoptosis by targeting the Notch signaling pathway in podocytes.Experimental and therapeutic medicine · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have been indicated that tumor necrosis factor receptor-associated factor 6 (TRAF6)-induced inflammation leads to acute kidney injury (AKI). How microRNA (miR) contributes to this process is poorly defined. The aim of this study was to investigate whether miR-590-3p regulated lipopolysaccharide (LPS)-induced inflammatory response by inhibiting TRAF6. LPS-induced septic mice were treated with adenovirus expressing miR-590-3p (ad-miR-590-3p) via tail-vein injection. AKI was evaluated by examining serum cystatin C (CysC), serum β2-microglobulin (β2-MG), and blood urea nitrogen (BUN). The mRNA and protein levels were assayed by RT-qPCR and western blotting, respectively. The proliferation of podocytes was monitored using the MTT assay. Cell apoptosis was analyzed by flow cytometry. Survival outcomes in ad-miR-590-3p-transfected septic mice were markedly improved compared with mice with LPS-induced sepsis. Ad-miR-590-3p transfection significantly attenuated LPS-induced AKI, which was reflected by an improved glomerular filtration rate (GFR) as determined by measuring CysC, β2-MG, and BUN. Moreover, we observed that miR-590-3p was a novel regulator of TRAF6, binding to its 3'-untranslated regions (3'-UTRs). In vitro, a miR-590-3p gain-of-function mutation blocked LPS-induced podocyte growth inhibition and apoptosis, as well as overactivation of the inflammatory response. miR-590-3p has the ability to suppress LPS-induced AKI and podocyte apoptosis by targeting TRAF6. This might provide a novel strategy for the treatment of LPS-induced renal injuries.
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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.