ArticleHuman cell2022
Long noncoding RNA MIR3142HG accelerates lipopolysaccharide-induced acute lung injury via miR-95-5p/JAK2 axis.
Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Bioinformatic Analysis and Experimental Verification Reveal the Protective Role of Baicalein Against LPS-Induced Endothelial Cell Dysfunction.Journal of inflammation research · 2026Article
- IL-6-induced long noncoding RNA MIR3142HG promotes tumorigenesis by interacting with thioredoxin-1 and STAT3 in human colorectal cancer.Cellular & molecular biology letters · 2025Article
- Assessment of MIR3142HG genetic polymorphisms and the susceptibility of lumbar disc herniation in the Chinese population.Scientific reports · 2024Article
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- Molecular mechanisms of Sepsis attacking the immune system and solid organs.Frontiers in medicine · 2024Review
- Insight into the lncRNA-mRNA Co-Expression Profile and ceRNA Network in Lipopolysaccharide-Induced Acute Lung Injury.Current issues in molecular biology · 2023Article
- Evaluation of the prognostic value of lncRNA UCA1 combined with extravascular lung water index and lung ultrasound score in patients with acute lung injury.The clinical respiratory journal · 2023Article
- Inhibition of gp130 alleviates LPS-induced lung injury by attenuating apoptosis and inflammation through JAK1/STAT3 signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
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
The study aims to clarify the expression pattern of MIR3142HG in acute lung injury (ALI) and investigate the potential mechanisms for the regulatory role of MIR3142HG in JAK/STAT in ALI. Notably, the ALI patients presented the overexpression of MIR3142HG and JAK2 in their serum samples. Knockdown of MIR3142HG facilitated cell viability but impaired cell apoptosis and inflammatory response via targeting miR-95-5p in lipopolysaccharide (LPS)-treated ALI cells. Overexpression of miR-95-5p promoted cell viability but suppressed apoptosis and inflammatory response via targeting JAK2 in LPS-induced ALI cells. The rescue experiments indicated that inhibition of miR-95-5p could reverse the increased cell viability and promote the inhibited apoptosis and inflammatory response induced by MIR3142HG knockdown in LPS-induced ALI. In conclusion, MIR3142HG is increased in sepsis-induced ALI, and MIR3142HG could accelerate the progression of sepsis-induced ALI through miR-95-5p/JAK2 axis, providing theoretical evidence for MIR3142HG to be a promising target for the therapeutics of ALI.
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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 Socratic graph.