Evidence map›Paper›PMID 36572901›Full record

ArticleJournal of translational medicine2022

Protective effects of Gypenoside XVII against cerebral ischemia/reperfusion injury via SIRT1-FOXO3A- and Hif1a-BNIP3-mediated mitochondrial autophagy.

Weijie Xie, Ting Zhu, Shuxia Zhang, Xiaobo Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

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  5. Interplay between ischemia-reperfusion and metabolic reprogramming.Apoptosis : an international journal on programmed cell death · 2026
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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

4 authors at 4 institutions in 1 country.

Weijie Xie *Research Center for Pharmacology and Toxicology, Institute of Medicinal Plant Development, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100193, China.
Ting Zhu *Research Center for Pharmacology and Toxicology, Institute of Medicinal Plant Development, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100193, China.
Shuxia ZhangResearch Center for Pharmacology and Toxicology, Institute of Medicinal Plant Development, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100193, China.
Xiaobo SunResearch Center for Pharmacology and Toxicology, Institute of Medicinal Plant Development, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100193, China. sun-xiaobo@163.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNShanghai Mental Health Center · CNState Administration of Traditional Chinese Medicine of the People's Republic of China · CNTechnology and Engineering Center for Space Utilization · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondrial autophagy maintains mitochondrial function and cellular homeostasis and plays a critical role in the pathological process of cerebral ischemia/reperfusion injury (CIRI). Whether Gypenoside XVII (GP17) has regulatory effects on mitochondrial autophagy against CIRI remains unclear. The purpose of this study was to investigate the pharmacodynamic effects and mechanisms of GP17 on mitochondrial autophagy after CIRI.

methodsA rat middle cerebral artery occlusion/reperfusion (MCAO/R) model was used to assess the effects of GP17 against CIRI and to explore the underlying mechanisms. An oxygen-glucose deprivation/reoxygenation (OGD/R) cell model was used to verify the ameliorative effects on mitochondrial damage and to probe the autophagy pathways involved in combating neural injuries.

resultsThe in vivo results showed that GP17 significantly improved mitochondrial metabolic functions and suppressed cerebral ischemic injury, possibly via the autophagy pathway. Further research revealed that GP17 maintains moderate activation of autophagy under ischemic and OGD conditions, producing neuroprotective effects against CIRI, and that the regulation of mitochondrial autophagy is associated with crosstalk between the SIRT1-FOXO3A and Hif1a-BNIP3 signalling pathway that is partially eliminated by the specific inhibitors AGK-7 and 2-ME.

conclusionOverall, this work offers new insights into the mechanisms by which GP17 protects against CIRI and highlights the potential of therapy with Notoginseng leaf triterpene compounds as a novel clinical strategy in humans.

Indexed as

Brain IschemiaReperfusion InjuryAnimalsApoptosisAutophagyHumansHypoxia-Inducible Factor 1, alpha SubunitInfarction, Middle Cerebral ArteryMembrane ProteinsMitochondriaMitochondrial ProteinsProto-Oncogene ProteinsRatsSaponinsSirtuin 1BNIP3 protein, humanBNIP3 protein, ratgypenoside XVIIHIF1A protein, humanHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsMitochondrial ProteinsProto-Oncogene ProteinsSaponinsSIRT1 protein, humanSirt1 protein, ratSirtuin 1BNIP3Cerebral ischemia/reperfusion injuryFOXO3AGypenoside XVIIMitochondrial autophagy

Identifiers

PMID36572901
PMCPMC9793669
OpenAlexW4312198479

What OpenQuestion 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 OpenQuestion graph.