Evidence map›Paper›PMID 36611931›Full record

ArticleCells2022

Notch1 Protects against Ischemic-Reperfusion Injury by Suppressing PTEN-Pink1-Mediated Mitochondrial Dysfunction and Mitophagy.

Qirong Xu, Sheng Liu, Qiang Gong, Rongrong Zhu, Jichun Liu, Qicai Wu, Xueliang Zhou

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2022. 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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026
    Review
  4. Article
  5. Article
  6. Article
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  8. Review
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  14. Review
  15. Article
  16. Mitophagy for cardioprotection.Basic research in cardiology · 2023
    Review
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Qirong XuDepartment of Thoracic Surgery, The First Affiliated Hospital, Nanchang University, Nanchang 330006, China.
Sheng LiuDepartment of Cardiac Surgery, The First Affiliated Hospital, Nanchang University, Nanchang 330006, China.
Qiang GongDepartment of Cardiac Surgery, The First Affiliated Hospital, Nanchang University, Nanchang 330006, China.
Rongrong ZhuDepartment of Cardiology, Jiangxi Hospital of Traditional Chinese Medicine, Jiangxi University of Chinese Medicine, Nanchang 330006, China.
Jichun LiuDepartment of Cardiac Surgery, The First Affiliated Hospital, Nanchang University, Nanchang 330006, China.
Qicai WuDepartment of Cardiac Surgery, The First Affiliated Hospital, Nanchang University, Nanchang 330006, China.
Xueliang ZhouDepartment of Cardiac Surgery, The First Affiliated Hospital, Nanchang University, Nanchang 330006, China.ORCID 0000-0003-2879-2882
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial ischemia/reperfusion injury is associated with adverse cardiovascular outcomes after acute myocardial infarction. However, the molecular mechanism of ischemia/reperfusion injury remains unclear. Mitochondria dysfunction is a participant in and regulator of myocardial ischemia-reperfusion injury. However, the molecular mechanisms involved in this process are not yet fully understood. We previously reported that Notch1 can reduce mitochondrial lysis, reduce myocardial infarct size, and inhibit ventricular remodeling. Herein, we explore the role of the downstream target Notch1 in mitochondrial regulation.

methodsThis study constructs an ischemic/reperfusion injury rat model and a hypoxia/reoxygenation cell model. The expression of PTEN is detected by real-time PCR, Western blot, and immunofluorescence staining. Cell viability is analyzed with CCK-8. Apoptosis level is detected via the TUNEL assay, and mitochondrial fission/fusion is analyzed with MitoTracker Green staining. Cardiac troponin I (cTnI), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and CK levels of creatine kinase-MB (CK) are measured with ELISA kits.

resultsWe found that PETN-Pink1-Parkin signaling is inhibited by Notch1 I/R in injured neonatal cardiomyocytes and hearts, i.e., via the inhibition of mitochondrial dysfunction and fragmentation. With the recure of PTEN or Pink1, the protective effect of Notch1 was largely diminished.

conclusionThese results suggest that N1ICD acts protectively against ischemic reperfusion injury by suppressing PTEN-Pink1-mediated mitochondrial dysfunction and fragmentation.

Indexed as

MitophagyMyocardial Reperfusion InjuryAnimalsApoptosisHumansMitochondriaMyocytes, CardiacPTEN-Induced Putative KinasePTEN PhosphohydrolaseRatsReceptor, Notch1NOTCH1 protein, humanNotch1 protein, ratPTEN-Induced Putative KinasePTEN PhosphohydrolasePTEN protein, humanPten protein, ratReceptor, Notch1ischemic-reperfusion injuryNotch1Pink1-Mfn2-ParkinPTEN

Identifiers

PMID36611931
PMCPMC9818205
OpenAlexW4313360928

What OpenQuestion holds

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LicenceCC BY
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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.