ArticleJournal of inflammation (London, England)2021
LncRNA TUG1 regulates the development of ischemia-reperfusion mediated acute kidney injury through miR-494-3p/E-cadherin axis.
Article in Journal of inflammation (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- lncRNA SND1-IT1/miR-494-3p regulation in ox-LDL-induced endothelial cell injury: novel insights into coronary heart disease pathogenesis and diagnostic biomarkers.European journal of medical research · 2026Article
- Emerging Frontiers in acute kidney injury: The role of extracellular vesicles.Bioactive materials · 2025Review
- The role of lncRNAs in AKI and CKD: Molecular mechanisms, biomarkers, and potential therapeutic targets.Genes & diseases · 2025Review
- Efficacy of exosomes in acute kidney injury treatment and the associated mechanism (Review).Molecular medicine reports · 2025Review
- lncRNA TUG1 and kidney diseases.BMC nephrology · 2025Review
- Enhancement of YTHDF2 plays a protective role in acute IRI models through downregulation of TUG1 expression.PloS one · 2025Article
- Pseudogene GSTM3P1 derived long non-coding RNA promotes ischemic acute kidney injury by target directed microRNA degradation of kidney-protective mir-668.Kidney international · 2024Article
- The role of non-protein-coding RNAs in ischemic acute kidney injury.Frontiers in immunology · 2024Review
- Discovery of mmu-lncRNA129814/hsa-lncRNA582795 as a Potential Biomarker and Intervention Target for Ischemia Reperfusion Injury-Induced AKI.Journal of inflammation research · 2024Article
- LncRNAs in oncogenic microenvironment: from threat to therapy.Frontiers in cell and developmental biology · 2024Review
- Review
- Syndecan-1 shedding destroys epithelial adherens junctions through STAT3 after renal ischemia/reperfusion injury.iScience · 2023Article
- Exosomes Highlight Future Directions in the Treatment of Acute Kidney Injury.International journal of molecular sciences · 2023Review
- MicroRNAs as Biomarkers and Therapeutic Targets for Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2023Review
- Long Non-Coding RNAs in Hypoxia and Oxidative Stress: Novel Insights Investigating a Piglet Model of Perinatal Asphyxia.Biology · 2023Article
- Article
- mmu-lncRNA 121686/hsa-lncRNA 520657 induced by METTL3 drive the progression of AKI by targeting miR-328-5p/HtrA3 signaling axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- LncRNA ENSMUST_147219 mediates the progression of ischemic acute kidney injury by targeting the miR-221-5p/IRF6 axis.Apoptosis : an international journal on programmed cell death · 2022Article
- Exosomal lncRNA TUG1 derived from human urine-derived stem cells attenuates renal ischemia/reperfusion injury by interacting with SRSF1 to regulate ASCL4-mediated ferroptosis.Stem cell research & therapy · 2022Article
- An update on the functional roles of long non‑coding RNAs in ischemic injury (Review).International journal of molecular medicine · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAcute kidney injury (AKI) results from renal dysfunction caused by various causes, resulting in high mortality. The underlying mechanisms of ischemia-reperfusion (I/R) induced AKI is very complicated and needed for further research. Here, we sought to found out the functions of lncRNA TUG1 in I/R-induced AKI.
methodsIn vivo model was constructed by I/R-induced mice and in vitro model was constructed by hypoxia/reoxygenation (H/R)-induced HK-2 cell. Kidney tissue damage was evaluated through H&E staining in mice. Cell flow cytometry was used to detect the degree of apoptosis. TUG1, miR-494-3p and E-cadherin were determined both by RT-PCR and western blot. Dual luciferase assay was employed to validate the relationships between TUG1, miR-494-3p and E-cadherin. Inflammatory factors including IL-1β, TNFɑ and IL-6 were evaluated by ELISA.
resultslncRNA TUG1 was decreased while miR-494-3p was elevated in vivo and in vitro. Overexpression of TUG1 or transfection with miR-494-3p inhibitor significantly alleviated cell apoptosis. MiR-494-3p directly targeted E-cadherin and TUG1 suppressed cell apoptosis via serving as a miR-494-3p sponge to disinhibit E-cadherin.
conclusionlncRNA TUG1 alleviated I/R-induced AKI through targeting miR-494-3p/E-cadherin.
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Registered trials
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