Evidence map›Paper›PMID 37194759›Full record

ArticleActa cirurgica brasileira2023

Remote ischemic preconditioning-induced late cardioprotection: possible role of melatonin-mitoKATP-H2S signaling pathway.

Haizhao Zhang, Shuang Li, Yu Jin

Open access · goldAbstract read
In one paragraph

Article in Acta cirurgica brasileira, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Crosstalk Between HHandbook of experimental pharmacology · 2026
    Review
  2. Review
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

3 authors at 2 institutions in 1 country.

Haizhao ZhangShenzhen Qianhai Shekou Free Trade Zone Hospital - Department of Cardiology - Shenzhen, China.ORCID http://orcid.org/0009-0000-9895-3093
Shuang LiShenzhen Qianhai Shekou Free Trade Zone Hospital - Department of Ophthalmology - Shenzhen, China.ORCID http://orcid.org/0009-0009-4671-9698
Yu JinShenzhen Second People's Hospital - Department of Cardiology - Shenzhen, China.ORCID http://orcid.org/0000-0002-6031-7005
Guangzhou Development Zone Hospital · CNShenzhen Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeRemote ischemic preconditioning (RIPC) confers cardioprotection against ischemia reperfusion (IR) injury. However, the precise mechanisms involved in RIPC-induced cardioprotection are not fully explored. The present study was aimed to identify the role of melatonin in RIPC-induced late cardioprotective effects in rats and to explore the role of H2S, TNF-α and mitoKATP in melatonin-mediated effects in RIPC.

methodsWistar rats were subjected to RIPC in which hind limb was subjected to four alternate cycles of ischemia and reperfusion of 5 min duration by using a neonatal blood pressure cuff. After 24 h of RIPC or ramelteon-induced pharmacological preconditioning, hearts were isolated and subjected to IR injury on the Langendorff apparatus.

resultsRIPC and ramelteon preconditioning protected the hearts from IR injury and it was assessed by a decrease in LDH-1, cTnT and increase in left ventricular developed pressure (LVDP). RIPC increased the melatonin levels (in plasma), H2S (in heart) and decreased TNF-α levels. The effects of RIPC were abolished in the presence of melatonin receptor blocker (luzindole), ganglionic blocker (hexamethonium) and mitochondrial KATP blocker (5-hydroxydecanoic acid).

conclusionsRIPC produce delayed cardioprotection against IR injury through the activation of neuronal pathway, which may increase the plasma melatonin levels to activate the cardioprotective signaling pathway involving the opening of mitochondrial KATP channels, decrease in TNF-α production and increase in H2S levels. Ramelteon-induced pharmacological preconditioning may also activate the cardioprotective signaling pathway involving the opening of mitochondrial KATP channels, decrease in TNF-α production and increase in H2S levels.

Indexed as

Ischemic PreconditioningIschemic Preconditioning, MyocardialMelatoninMyocardial InfarctionMyocardial Reperfusion InjuryAnimalsIndenesIschemiaKATP ChannelsPotassium ChannelsRatsRats, WistarSignal TransductionTumor Necrosis Factor-alphaIndenesKATP ChannelsMelatoninmitochondrial K(ATP) channelPotassium ChannelsramelteonTumor Necrosis Factor-alpha

Identifiers

PMID37194759
PMCPMC10191159
OpenAlexW4376608882

What OpenQuestion holds

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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 OpenQuestion graph.