Evidence map›Paper›PMID 29566706›Full record

ArticleJournal of translational medicine2018

Dexmedetomidine attenuates lung apoptosis induced by renal ischemia-reperfusion injury through α

Juanjuan Li, Qian Chen, Xinhai He, Azeem Alam, Jiaolin Ning, Bin Yi, Kaizhi Lu, Jianteng Gu

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

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  11. Alveolar macrophages polarization switch via αInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Juanjuan LiDepartment of Anesthesiology, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Road, Chongqing, 400038, China.
Qian ChenDepartment of Anesthesiology, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Road, Chongqing, 400038, China.
Xinhai HeDepartment of Anesthesiology, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Road, Chongqing, 400038, China.
Azeem AlamAnaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea & Westminster Campus, London, UK.
Jiaolin NingDepartment of Anesthesiology, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Road, Chongqing, 400038, China.
Bin YiDepartment of Anesthesiology, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Road, Chongqing, 400038, China.
Kaizhi LuDepartment of Anesthesiology, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Road, Chongqing, 400038, China.
Jianteng GuDepartment of Anesthesiology, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Road, Chongqing, 400038, China. jiantenggu@hotmail.com.ORCID 0000-0001-8418-9864
Army Medical University · CNImperial College London · GB

Funding

The National Natural Science Foundation of China 81272068The National Natural Science Foundation of China 81772050
6 · The paper itself

Abstract

backgroundAcute lung injury caused by renal ischemia-reperfusion is one of the leading causes of acute kidney injury-related death. Dexmedetomidine, an α

methodsIn vivo, acute kidney injury was induced by 60 min of kidney ischemia (bilateral occlusion of renal pedicles) followed by 24 h of reperfusion. Mice received dexmedetomidine (25 µg/kg, i.p.) in the absence or presence of α

resultsIn vivo, dexmedetomidine remarkably mitigated pathohistological changes and apoptosis and significantly increased p-Akt expression in the lung. In addition, dexmedetomidine also slightly improved oxygenation in mice after IR, which can be abolished by atipamezole. In vitro, dexmedetomidine significantly inhibited IR serum-induced loss of viability and apoptosis in PMVECs. Dexmedetomidine increased p-Akt in a time- and dose-dependent manner, and down-regulated the expression of caspase 3 and Bax and up-regulated the Bcl-2 expression in PMVECs. The changes of MMP were also improved by dexmedetomidine. Whilst these effects were abolished by Atipamezole or LY294002.

conclusionOur results demonstrated that dexmedetomidine attenuates lung apoptosis induced by IR, at least in part, via α

Indexed as

AnimalsApoptosisBlood Gas AnalysisCell SurvivalDexmedetomidineEndothelial CellsKidneyLungMaleMice, Inbred C57BLPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktReceptors, Adrenergic, alpha-2Reperfusion InjurySignal TransductionDexmedetomidinePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Adrenergic, alpha-2Acute lung injuryAkt pathwayApoptosisRenal ischemia–reperfusionα2-Adrenoceptor

Identifiers

PMID29566706
PMCPMC5865375
OpenAlexW2803570246

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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.