ArticleAmerican journal of translational research2021
Up-regulation of TUG1 can regulate miR-494/PDK4 axis to inhibit LPS-induced acute lung injury caused by sepsis.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- LncRNA TUG1 mitigates sepsis-induced acute lung injury via a ceRNA network regulating the CALM1/PRKG1/RYR3/AQP5 axis.Scientific reports · 2026Article
- Diagnostic and Prognostic Value of Deregulated Circulating Long Non-coding RNA TUG1 in Elderly Patients with Severe Pneumonia.Inflammation · 2023Article
- Fighting Fire with Fire: Exosomes and Acute Pancreatitis-Associated Acute Lung Injury.Bioengineering (Basel, Switzerland) · 2022Review
- Non-Coding RNA Networks as Potential Novel Biomarker and Therapeutic Target for Sepsis and Sepsis-Related Multi-Organ Failure.Diagnostics (Basel, Switzerland) · 2022Review
- Evaluating the potency of blood long noncoding RNA PVT1 as candidate biomarker reflecting inflammation, multiple organ dysfunction, and mortality risk in sepsis patients.Journal of clinical laboratory analysis · 2022Article
- LncRNA NEAT1 Potentiates SREBP2 Activity to Promote Inflammatory Macrophage Activation and Limit Hantaan Virus Propagation.Frontiers in microbiology · 2022Article
Corrections and comments
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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 lung injury (ALI) caused by sepsis is the most common disease and the leading cause of death in intensive care units. Recent studies have revealed that long non-coding RNAs (LncRNAs) are abnormally expressed in sepsis. This study aimed to clarify the role and mechanism of Taurine up-regulated gene 1 (TUG1) in ALI caused by sepsis.
methodsLipopolysaccharide (LPS) was used to simulate sepsis-induced ALI model. RT-PCR, Dual luciferase reporter (DLR) assay and RNA immunoprecipitation (RIP) were used to detect TUG1 and miR-494. The rat model with sepsis-induced ALI was established by intraperitoneal injection of LPS to verify the results of
resultsThe expressions of TUG1 and PDK4 were down-regulated while the expression of miR-494 was up-regulated in lung tissues and human small airway epithelial cells (HSAECs). TUG1 was indirectly mediated. Overexpression of TUG1 or inhibition of miR-494 could significantly improve the survival rate of HSAECs. Transfection of miR-494 mimics achieved the opposite effect. Enzyme-linked immunosorbent assay (ELISA) showed that the expression of arthritis-related factors in rats was increased after up-regulating TUG1.
conclusionTUG1 is lowly expressed in sepsis. Up-regulating TUG1 can alleviate the inflammatory response in ALI caused by LPS-induced sepsis, which may be a clinical treatment target.
Indexed as
Identifiers
34956459PMC8661222W4206887700What Socratic holds
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 Socratic graph.