Evidence map›Paper›PMID 24987958›Full record

ArticlePloS one2014

miR-146a ameliorates liver ischemia/reperfusion injury by suppressing IRAK1 and TRAF6.

Weiwei Jiang, Liangliang Kong, Qingfeng Ni, Yeting Lu, Wenzhou Ding, Guoqing Liu, Liyong Pu, Weibing Tang, Lianbao Kong

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
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  3. miRNA in the Progression of Diabetic Kidney Disease: New Insight.International journal of molecular sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Weiwei JiangDepartment of Neonatal Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Liangliang KongDepartment of Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qingfeng NiDepartment of Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yeting LuDepartment of Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wenzhou DingDepartment of Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Guoqing LiuDepartment of Neonatal Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Liyong PuDepartment of Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Weibing TangDepartment of Neonatal Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Lianbao KongDepartment of Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jiangsu Province Hospital · CNNanjing Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A critical role of the Toll-like receptor(TLR) and its downstream molecules, including IL-1 receptor-associated kinase 1(IRAK1) and tumor necrosis factor receptor- associated factor 6(TRAF6), in the pathogenesis of liver ischemia/reperfusion (I/R) injury has been documented. Recently a microRNA, miR-146a, was identified as a potent negative regulator of the TLR signaling pathway. In this study, we investigated the role of miR-146a to attenuate TLR signaling and liver I/R injury in vivo and in vitro. miR-146a was decreased in mice Kupffer cells following hepatic I/R, whereas IRAK1 and TRAF6 increased. Overexpression of miR-146a directly decreased IRAK1 and TRAF6 expression and attenuated the release of proinflammatory cytokines through the inactivation of NF-κB P65 in hypoxia/reoxygenation (H/R)-induced macrophages, RAW264.7 cells. Knockdown experiments demonstrated that IRAK1 and TRAF6 are two potential targets for reducing the release of proinflammatory cytokines. Moreover, co-culture assays indicated that miR-146a decreases the apoptosis of hepatocytes after H/R. In vivo administration of Ago-miR-146a, a stable version of miR-146a in vivo, protected against liver injury in mice after I/R via inactivation of the TLR signaling pathway. We conclude that miR-146a ameliorates liver ischemia/reperfusion injury in vivo and hypoxia/reoxygenation injury in vitro by directly suppressing IRAK1 and TRAF6.

Indexed as

Down-RegulationAnimalsCell HypoxiaCell LineHepatic InsufficiencyInflammationInterleukin-1 Receptor-Associated KinasesLiverMacrophagesMaleMice, Inbred C57BLMicroRNAsReperfusion InjurySignal TransductionTNF Receptor-Associated Factor 6Toll-Like ReceptorsInterleukin-1 Receptor-Associated KinasesIrak1 protein, mouseMicroRNAsMirn146 microRNA, mouseTNF Receptor-Associated Factor 6Toll-Like Receptors

Identifiers

PMID24987958
PMCPMC4079695
OpenAlexW2039118309

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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 OpenQuestion graph.