Evidence map›Paper›PMID 34145219›Full record

ArticleCell death & disease2021

Hypoxic postconditioning promotes mitophagy against transient global cerebral ischemia via PINK1/Parkin-induced mitochondrial ubiquitination in adult rats.

Haixia Wen, Luxi Li, Lixuan Zhan, Yunyan Zuo, Kongping Li, Meiqian Qiu, Heying Li, Weiwen Sun, En Xu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

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  15. Inhibition of SCFCommunications biology · 2025
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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

9 authors at 4 institutions in 1 country.

Haixia Wen *Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China.
Luxi Li *Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China.
Lixuan Zhan *Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China.
Yunyan ZuoInstitute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China.
Kongping LiInstitute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China.
Meiqian QiuInstitute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China.
Heying LiGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
Weiwen SunInstitute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China.
En XuInstitute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, P. R. China. enxu@163.net.
Guangzhou Medical University · CNGuangdong 999 Brain Hospital · CNGuangzhou First People's Hospital · CNGuangzhou Institutes of Biomedicine and Health · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81873745National Natural Science Foundation of China (National Science Foundation of China) 81971124National Natural Science Foundation of China (National Science Foundation of China) 82071281
6 · The paper itself

Abstract

Mitophagy alleviates neuronal damage after cerebral ischemia by selectively removing dysfunctional mitochondria. Phosphatase and tensin homolog (PTEN) induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy is the most well-known type of mitophagy. However, little is known about the role of PINK1/Parkin-mediated mitophagy in ischemic tolerance induced by hypoxic postconditioning (HPC) with 8% O

Indexed as

MitophagyAnimalsCA1 Region, HippocampalDisease Models, AnimalHypoxiaIschemic Attack, TransientMaleMitochondriaNeuronsProtein KinasesProtein TransportPTEN-Induced Putative KinaseRatsRats, WistarUbiquitinationUbiquitin-Protein Ligasesparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein Ligases

Identifiers

PMID34145219
PMCPMC8213752
OpenAlexW3169757791

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.