ArticleMediators of inflammation2020
MEG3 Alleviated LPS-Induced Intestinal Injury in Sepsis by Modulating miR-129-5p and Surfactant Protein D.
Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Epigenetic mechanism of HDAC5 in sepsis-induced acute intestinal injury through KLF4-mediated intestinal epithelial cell ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Global research trends in non-coding RNA and intestinal epithelial homeostasis: an integrated bibliometric analysis (2007-2024).Hereditas · 2025Article
- LPS-induced extracellular AREG triggers macrophage pyroptosis through the EGFR/TLR4 signaling pathway.Frontiers in immunology · 2025Article
- Hippocampal adenosine-to-inosine RNA editing in sepsis: dynamic changes and influencing factors.Brain communications · 2024Article
- Long Noncoding RNA, MicroRNA, Zn Transporter Zip14 (Slc39a14) and Inflammation in Mice.Nutrients · 2022Article
- MiR-129-5p Inactivates NF-Journal of healthcare engineering · 2022Article
- Mechanism of M2 macrophage-derived extracellular vesicles carrying lncRNA MEG3 in inflammatory responses in ulcerative colitis.Bioengineered · 2021Article
- MicroRNA‑129 plays a protective role in sepsis‑induced acute lung injury through the suppression of pulmonary inflammation via the modulation of the TAK1/NF‑κB pathway.International journal of molecular medicine · 2021Article
- Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis and intestinal injury triggered by sepsis are common in intensive care units, which can contribute to a high mortality. lncRNAs can modulate gene expression, and they are closely involved in multiple diseases, including sepsis. In our present study, we investigated the biological function of MEG3 in sepsis, especially during the intestinal injury. Currently, we observed that in LPS-induced sepsis mouse models, the intestinal injury was triggered. Meanwhile, we reported that MEG3 was greatly decreased in vivo, with an increase of miR-129-5p and inhibition of SP-D. Then, MEG3 was overexpressed, and we found that its overexpression repressed the intestinal injury via downregulating miR-129-5p in sepsis mice. Moreover, TNF-
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