Evidence map›Paper›PMID 33758383›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2021

6-Gingerol relieves myocardial ischaemia/reperfusion injury by regulating lncRNA H19/miR-143/ATG7 signaling axis-mediated autophagy.

Xiang-Wei Lv, Meng-Jie Wang, Qiu-Yu Qin, Pan Lu, Guo-Wei Qin

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2021. 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  12. Article
  13. 6-gingerol and its derivatives inhibitFrontiers in microbiology · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. The regulatory roles of circular RNAsFrontiers in neurology · 2022
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Xiang-Wei LvDepartment of Cardiology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, P.R. China.
Meng-Jie WangDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Qiu-Yu QinDepartment of Cardiology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, P.R. China.
Pan LuDepartment of Cardiology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, P.R. China.
Guo-Wei QinDepartment of Science and Technology, Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, P.R. China. qinguowei@glmc.edu.cn.
Guilin Medical University · CNThe People's Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischemia/reperfusion injury (MIRI) causes severe damage in cardiac tissue, thereby resulting in a high rate of mortality. 6-Gingerol (6-G) is reported to play an essential role in alleviating MIRI. However, the underlying mechanism remains obscure. This study was intended to explore the potential mechanism by which 6-G functions. Q-PCR was employed to quantify the relative RNA levels of long noncoding RNA (lncRNA) H19 (H19), miR-143, and ATG7, an enzyme essential for autophagy, in HL-1 cells. Western blotting, immunofluorescence, and immunohistochemistry were employed for protein evaluation in cultured cells or mouse tissues. Cell viability, cytotoxicity, and apoptosis were analysed by CCK-8, LDH, and flow cytometry assays, respectively. The binding sites for miR-143 were predicted using starBase software and experimentally validated through a dual-luciferase reporter system. Here, we found that 6-G elevated cellular H19 expression in hypoxia/reoxygenation (H/R)-treated HL-1 cells. Moreover, 6-G increased Bcl-2 expression but reduced cleaved caspase 3 and caspase 9 protein levels. Mechanistically, H19 directly interacted with miR-143 and lowered its cellular abundance by acting as a molecular sponge. Importantly, ATG7 was validated as a regulated gene of miR-143, and the depletion of miR-143 by H19 caused an increased in ATG7 expression, which in turn promoted the autophagy process. Last, mouse experiments highly supported our in vitro findings that 6-G relieves MIRI by enhancing autophagy. The H19/miR-143/ATG7 axis was shown to be critical for the function of 6-G in relieving MIRI.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 7CatecholsCell LineFatty AlcoholsMaleMiceMice, Inbred C57BLMicroRNAsMyocardial Reperfusion InjuryRNA, Long NoncodingSignal TransductionAtg7 protein, mouseAutophagy-Related Protein 7CatecholsFatty AlcoholsgingerolH19 long non-coding RNAMicroRNAsMIRN143 microRNA, mouseRNA, Long Noncoding

Identifiers

PMID33758383
OpenAlexW3138784739

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.