Evidence map›Paper›PMID 31680420›Full record

ArticleJournal of cellular and molecular medicine2020

Dexmedetomidine post-treatment attenuates cardiac ischaemia/reperfusion injury by inhibiting apoptosis through HIF-1α signalling.

Ke Peng, Wei-Rong Chen, Fan Xia, Hong Liu, Xiao-Wen Meng, Juan Zhang, Hua-Yue Liu, Zheng-Yuan Xia, Fu-Hai Ji

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 48 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

9 authors at 2 institutions in 2 countries.

Ke PengDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Wei-Rong ChenDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Fan XiaDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Hong LiuDepartment of Anesthesiology and Pain Medicine, University of California Davis Health, Sacramento, CA, USA.
Xiao-Wen MengDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Juan ZhangDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Hua-Yue LiuDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.
Zheng-Yuan XiaDepartment of Anesthesiology and Pain Medicine, University of California Davis Health, Sacramento, CA, USA.
Fu-Hai JiDepartment of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0001-6649-665X
Soochow University · CNUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia-inducible factor 1α (HIF-1α) plays a critical role in the apoptotic process during cardiac ischaemia/reperfusion (I/R) injury. This study aimed to investigate whether post-treatment with dexmedetomidine (DEX) could protect against I/R-induced cardiac apoptosis in vivo and in vitro via regulating HIF-1α signalling pathway. Rat myocardial I/R was induced by occluding the left anterior descending artery for 30 minutes followed by 6-hours reperfusion, and cardiomyocyte hypoxia/reoxygenation (H/R) was induced by oxygen-glucose deprivation for 6 hours followed by 3-hours reoxygenation. Dexmedetomidine administration at the beginning of reperfusion or reoxygenation attenuated I/R-induced myocardial injury or H/R-induced cell death, alleviated mitochondrial dysfunction, reduced the number of apoptotic cardiomyocytes, inhibited the activation of HIF-1α and modulated the expressions of apoptosis-related proteins including BCL-2, BAX, BNIP3, cleaved caspase-3 and cleaved PARP. Conversely, the HIF-1α prolyl hydroxylase-2 inhibitor IOX2 partly blocked DEX-mediated cardioprotection both in vivo and in vitro. Mechanistically, DEX down-regulated HIF-1α expression at the post-transcriptional level and inhibited the transcriptional activation of the target gene BNIP3. Post-treatment with DEX protects against cardiac I/R injury in vivo and H/R injury in vitro. These effects are, at least in part, mediated via the inhibition of cell apoptosis by targeting HIF-1α signalling.

Indexed as

ApoptosisAdrenergic alpha-2 Receptor AgonistsAnimalsDexmedetomidineDisease Models, AnimalGene Expression RegulationHypoxia-Inducible Factor 1, alpha SubunitMaleMyocardial IschemiaMyocardial Reperfusion InjuryProtective AgentsRatsRats, Sprague-DawleyAdrenergic alpha-2 Receptor AgonistsDexmedetomidineHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitProtective Agentscardiac apoptosiscardioprotectiondexmedetomidineHIF-1αhypoxia/reoxygenationischaemia/reperfusion

Identifiers

PMID31680420
PMCPMC6933328
OpenAlexW2985249059

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.