Evidence map›Paper›PMID 25789157›Full record

ArticleCell & bioscience2015

Mediation of exogenous hydrogen sulfide in recovery of ischemic post-conditioning-induced cardioprotection via down-regulating oxidative stress and up-regulating PI3K/Akt/GSK-3β pathway in isolated aging rat hearts.

Hongzhu Li, Yuehong Wang, Can Wei, Shuzhi Bai, Yajun Zhao, Hongxia Li, Bo Wu, Rui Wang, Lingyun Wu, Changqing Xu

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 4% 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, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  8. Article
  9. Review
  10. Article
  11. The Cardiovascular Effects of Hydrogen Sulfide: The Epigenetic Mechanisms.Advances in experimental medicine and biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. HAging · 2019
    Article
  17. Review
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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

10 authors at 2 institutions in 2 countries.

Hongzhu LiDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Yuehong WangDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Can WeiDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Shuzhi BaiDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Yajun ZhaoDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Hongxia LiDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Bo WuDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Rui WangDepartment of Biology, Lakehead University, Thunder Bay, ON P7B5E1 Canada.
Lingyun WuDepartment of Health Science, Lakehead University, Thunder Bay, ON P7B5E1 Canada.
Changqing XuDepartment of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081 China.
Harbin Medical University · CNLakehead University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The physiological and pathological roles of hydrogen sulfide (H2S) in the regulation of cardiovascular functions have been recognized. Cystathionine gamma-lyase (CSE) is a major H2S-producing enzyme in cardiovascular system. Ischemic post-conditioning (PC) provides cadioprotection in young hearts but lost in the aging hearts. The involvement of H2S in the recovery of PC-induced cardioprotection in the aging hearts is unclear. In the present study, we demonstrated that ischemia/reperfusion (I/R) decreased H2S production rate and CSE expression, aggravated cardiomyocytes damage, apoptosis and myocardial infarct size, reduced cardiac function, increased the levels of Bcl-2, caspase-3 and caspase-9 mRNA, enhanced oxidative stress in isolated young and aging rat hearts. I/R also increased the release of cytochrome c and down-regulated the phosphorylation of PI3K, Akt and GSK-3β in the aging rat hearts. We further found that PC increased H2S production rate and CSE expressions, and protected young hearts from I/R-induced cardiomyocytes damage, all of which were disappeared in the aging hearts. Supply of NaHS not only increased PC-induced cardioprotection in the young hearts, but also lightened I/R induced-myocardial damage and significantly recovered the cardioprotective role of PC against I/R induced myocardial damage in the aging hearts. LY294002 (a PI3K inhibitor) abolished but N-acetyl-cysteine (NAC, an inhibitor of reactive oxygen species, ROS) further enhanced the protective role of H2S against I/R induced myocardial damage in the aging hearts. In conclusion, these results demonstrate that exogenous H2S recovers PC-induced cardioprotection via inhibition of oxidative stress and up-regulation of PI3K-Akt-GSK-3β pathway in the aging rat hearts. These findings suggested that H2S might be a novel target for the treatment of aging cardiovascular diseases.

Indexed as

Aging ratsCardiomyocytesHydrogen sulfideIschemic post-conditioningOxidative stress

Identifiers

PMID25789157
PMCPMC4364662
OpenAlexW2102983882

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.