Evidence map›Paper›PMID 32199783›Full record

ArticleRedox biology2020

Restoration of L-OPA1 alleviates acute ischemic stroke injury in rats via inhibiting neuronal apoptosis and preserving mitochondrial function.

Yongxing Lai, Peiqiang Lin, Manli Chen, Yixian Zhang, Jianhao Chen, Mouwei Zheng, Ji Liu, Houwei Du, Ronghua Chen, Xiaodong Pan and 2 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 90 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 3 pooled it
7.8field-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

90 citing papers in PubMed, 3 syntheses or guidelines pooled it, 159 citations in OpenAlex.

  1. Pooled it
  2. Lentivirus- or AAV-mediated gene therapy interventions in ischemic stroke: A systematic review of preclinicalJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Pooled it
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  4. Trial
  5. Article
  6. Article
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  8. Article
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  10. Impacts of Oxylipins on ischemic stroke: from pathophysiology to clinical phenotypes.Metabolomics : Official journal of the Metabolomic Society · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Spatial metabolic analysis of the regulatory effects of DL-3-n-butylphthalide in a cerebral ischemia-reperfusion mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  16. Article
  17. Review
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30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Yongxing LaiDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Department of Rehabilitation, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Peiqiang LinDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Department of Rehabilitation, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Manli ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Yixian ZhangDepartment of Rehabilitation, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Jianhao ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Mouwei ZhengDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Ji LiuDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Houwei DuDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Ronghua ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Xiaodong PanDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China.
Nan LiuDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Department of Rehabilitation, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China. Electronic address: xieheliunan1984@sina.com.
Hongbin ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Department of Rehabilitation, Fujian Medical University Union Hospital, Fuzhou, 350001, China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, 350001, China. Electronic address: 462501173@qq.com.
Union Hospital · CNFujian Medical University · CNFujian Institute of Microbiology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIschemic stroke can induce changes in mitochondrial morphology and function. As a regulatory gene in mitochondria, optic atrophy 1 (OPA1) plays a pivotal role in the regulation of mitochondrial dynamics and other related functions. However, its roles in cerebral ischemia-related conditions are barely understood.

methodsCultured rat primary cortical neurons were respectively transfected with OPA1-v1ΔS1-encoding and OPA1-v1-encoding lentivirus before exposure to 2-h oxygen-glucose deprivation (OGD) and subsequent reoxygenation (OGD/R). Adult male SD rats received an intracranial injection of AAV-OPA1-v1ΔS1 and were subjected to 90 min of transient middle cerebral artery occlusion (tMCAO) followed by reperfusion. OPA1 expression and function were detected by in vitro and in vivo assays.

resultsOPA1 was excessively cleaved after cerebral ischemia/reperfusion injury, both in vitro and in vivo. Under OGD/R condition, compared with that of the LV-OPA1-v1-treated group, the expression of OPA1-v1ΔS1 efficiently restored L-OPA1 level and alleviated neuronal death and mitochondrial morphological damage. Meanwhile, the expression of OPA1-v1ΔS1 markedly improved cerebral ischemia/reperfusion-induced motor function damage, attenuated brain infarct volume, neuronal apoptosis, mitochondrial bioenergetics deficits, oxidative stress, and restored the morphology of mitochondrial cristae and mitochondrial length. It also preserved the mitochondrial integrity and reinforced the mtDNA content and expression of mitochondrial biogenesis factors in ischemic rats.

interpretationOur results demonstrate that the stabilization of L-OPA1 protects ischemic brains by reducing neuronal apoptosis and preserving mitochondrial function, suggesting its significance as a promising therapeutic target for stroke prevention and treatment.

Indexed as

Brain IschemiaIschemic StrokeReperfusion InjuryStrokeAnimalsApoptosisGlucoseMaleMitochondriaRatsRats, Sprague-DawleyGlucoseApoptosisIschemia/reperfusionMitochondria functionOPA1Oxidative stress

Identifiers

PMID32199783
PMCPMC7327985
OpenAlexW3010792095

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.