Evidence map›Paper›PMID 31344138›Full record

ArticlePloS one2019

Dexmedetomidine-induced cardioprotection is mediated by inhibition of high mobility group box-1 and the cholinergic anti-inflammatory pathway in myocardial ischemia-reperfusion injury.

Juan Zhang, Fan Xia, Haifeng Zhao, Ke Peng, Huayue Liu, Xiaowen Meng, Chen Chen, Fuhai Ji

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.6field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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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 1 country.

Juan ZhangDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Fan XiaDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Haifeng ZhaoDepartment of Pathology, Suzhou Hospital Affiliated to Nanjing Medical University, Suzhou Science and Technology Town Hospital, Suzhou, China.
Ke PengDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Huayue LiuDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Xiaowen MengDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Chen ChenDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Fuhai JiDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0001-6649-665X
Soochow University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDexmedetomidine (DEX) is a selective α2-adrenoceptor agonist that has anti-inflammatory and cardioprotective effects in myocardial ischemia/reperfusion (I/R) injury. The present study aimed to investigate the underlying mechanism by which DEX protects against myocardial I/R.

methodsSprague Dawley rats were subjected to either sham operation or myocardial I/R, which was induced by ligating the left anterior descending coronary artery for 30 min followed by reperfusion for 120 min. Rats were treated with either DEX or saline prior to surgery. We measured heart infarct size, serum cardiac Troponin I (cTnI), cardiac High mobility group box-1 (HMGB1) expression, myocardial apoptosis and cytokine production of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Besides, we evaluated the heart function at 4 weeks post-reperfusion by echocardiography. Unilateral vagotomy or inhibition of the α7 nicotinic acetylcholine receptor (α7nAChR) with methyllycaconitine (MLA) was applied to investigate whether DEX-induced cardioprotection is mediated via the cholinergic anti-inflammatory pathway. Cardiac-selective overexpression of HMGB1 was administered to further confirm if HMGB1 is a key anti-inflammatory target during DEX-induced cardioprotection.

resultsDEX pretreatment significantly attenuated I/R-induced cardiac damage, as evidenced by decreases in short-term injury indicators including myocardial infarct size, cTnI release, myocardial apoptosis, cardiac HMGB1 expression, IL-6 and TNF-α production, as well as improvement on long-term cardiac function at 4 weeks post-reperfusion. These effects were partially reversed by either unilateral vagotomy or methyllycaconitine treatment. Besides, cardiac HMGB1-overexpression nearly abolished DEX-induced cardioprotection.

conclusionsDEX pretreatment protects against myocardial I/R by inhibiting cardiac HMGB1 production and activating the cholinergic anti-inflammatory pathway.

Indexed as

AnimalsCardiotonic AgentsDexmedetomidineGene Expression RegulationHMGB1 ProteinHumansInterleukin-6Myocardial Reperfusion InjuryMyocardiumNeuroimmunomodulationRatsSignal TransductionTroponin ITumor Necrosis Factor-alphaVagotomyCardiotonic AgentsDexmedetomidineHMGB1 ProteinInterleukin-6Troponin ITumor Necrosis Factor-alpha

Identifiers

PMID31344138
PMCPMC6657822
OpenAlexW2963491687

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.