ArticleCentral-European journal of immunology2022
Downregulation of lncRNA NEAT1 alleviates sepsis-induced acute kidney injury.
Article in Central-European journal of immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- The versatile roles of long non-coding RNAs in kidney disease.Nature reviews. Nephrology · 2026Review
- Identification and validation of lymphangiogenesis-related genes for predicting acute myeloid leukemia prognosis: insights from bulk RNA sequencing and single-cell RNA sequencing analyses.Clinical and experimental medicine · 2026Article
- Diagnostic Value and Mechanism of Action of LINC00641 in Sepsis-Associated Acute Kidney Injury.Journal of inflammation research · 2026Article
- Inflammation, cell death, and lncRNAs: unraveling the mechanisms of sepsis-associated acute kidney injury.Frontiers in immunology · 2026Review
- Review
- The NEAT1/miR-124-3p/CCL2 axis in chronic kidney disease progression: integrated bioinformatics analysis and experimental validation.Epigenomics · 2025Article
- Puerarin raises exosomal miR- 342 - 3p by inhibiting lncRNA NEAT1 in umbilical cord mesenchymal stem cells to alleviate renal tubular epithelial cell pyroptosis in chronic renal failure.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The role of lncRNAs in AKI and CKD: Molecular mechanisms, biomarkers, and potential therapeutic targets.Genes & diseases · 2025Review
- Critical role of LncRNA in sepsis-associated acute kidney injury.Frontiers in pharmacology · 2025Review
- LncRNA PCED1B-AS1 Inhibits Sepsis-Induced Acute Kidney Injury by Promoting Transformation of Macrophages from M1 to M2 Type via Regulating the miR-361-3p/SOCS1 Axis.Journal of inflammation research · 2025Article
- LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury.Scientific reports · 2024Article
- Long Non-coding RNA NEAT1 , NOD-Like Receptor Family Protein 3 Inflammasome, and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2024Article
- An updated review of the pharmacological effects and potential mechanisms of hederagenin and its derivatives.Frontiers in pharmacology · 2024Review
- Exploring the role of hyperforin in modulating the NF-κB/miR-21 axis in sepsis-induced acute kidney injury.Central-European journal of immunology · 2024Article
- LncRNA HCP5 acts as a potential diagnostic biomarker and attenuates the inflammatory response in neonatal sepsis by targeting miR-138-5p/SIRT1.Central-European journal of immunology · 2024Article
- MicroRNAs in septic acute kidney injury.Burns & trauma · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced acute kidney injury (AKI) is one of the important causes of increased mortality in sepsis patients. Long non-coding RNA (lncRNA) is believed to play a vital function in the progression of AKI. However, the mechanism of nuclear enriched abundant transcript 1 (NEAT1) has not been fully elucidated. NEAT1 was overexpressed and miR-22-3p was underexpressed in sepsis patients and lipopolysaccharide (LPS)-induced AKI cell models. Knockdown of NEAT1 could promote viability and suppress apoptosis and the inflammatory response in LPS-induced HK2 cells. MiR-22-3p could be sponged by NEAT1, and its inhibitor reversed the inhibition effect of NEAT1 silencing on LPS-induced HK2 cell injury. CXCL12 could be targeted by miR-22-3p, and its overexpression reversed the suppression effect of miR-22-3p on LPS-induced HK2 cell injury. Silenced NEAT1 could restrain the activity of the NF-κB signaling pathway, and miR-22-3p inhibitor or CXCL12 overexpression could reverse this effect. In addition, NEAT1 knockdown alleviated the inflammation response of cecal ligation and puncture (CLP) mouse models. In summary, our data showed that NEAT1 promoted LPS-induced HK2 cell injury via regulating the miR-22-3p/CXCL12/NF-κB signaling pathway, suggesting that NEAT1 knockdown might be a potential pathway for alleviating sepsis-induced AKI.
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