Evidence map›Paper›PMID 29796942›Full record

ArticleActa neurologica Belgica2020

Yap-Hippo pathway regulates cerebral hypoxia-reoxygenation injury in neuroblastoma N2a cells via inhibiting ROCK1/F-actin/mitochondrial fission pathways.

Chizi Geng, Jianchao Wei, Chengsi Wu

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Acta neurologica Belgica, 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 It has been retracted, and should not be counted.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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  11. (Z)-7,4'-dimethoxy-6-hydroxy-aurone-4-O-The Journal of international medical research · 2020
    Article
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  14. Role of YAP/TAZ in Energy Metabolism in the Heart.Journal of cardiovascular pharmacology · 2019
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Chizi GengPhysician of Neurology Department, Beijing Luhe Hospital, Capital Medical University, Beijing, China. gczzxc@163.com.
Jianchao WeiDirector of Neurology Department, Beijing Luhe Hospital, Capital Medical University, Beijing, China.
Chengsi WuDeputy Director of Eurology Department, Beijing Luhe Hospital, Capital Medical University, Beijing, China.
Beijing Luhe Hospital Affiliated to Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Yes-associated protein (Yap), a regulator of cellular apoptosis, has been demonstrated to be involved in cerebral ischemia-reperfusion (IR) injury through poorly defined mechanisms. The present study aimed to explore the role of Yap in regulating cerebral IR injury in vitro, with a focus on mitochondrial fission and ROCK1/F-actin pathways. Our data demonstrated that Yap was actually downregulated in N2a cells after cerebral hypoxia-reoxygenation (HR) injury, and that lower expression of Yap was closely associated with increased cell death. However, the reintroduction of Yap was able to suppress the HR-mediated N2a cells death via blocking the mitochondria-related apoptotic signal. At the molecular levels, Yap overexpression sustained mitochondrial potential, normalized the mitochondrial respiratory function, reduced ROS overproduction, limited HtrA2/Omi release from mitochondria into the nucleus, and suppressed pro-apoptotic proteins activation. Subsequently, functional studies have further illustrated that HR-mediated mitochondrial apoptosis was highly regulated by mitochondrial fission, whereas Yap overexpression was able to attenuate HR-mediated mitochondrial fission and, thus, promote N2a cell survival in the context of HR injury. At last, we demonstrated that Yap handled mitochondrial fission via closing ROCK1/F-actin signaling pathways. Activation of ROCK1/F-actin pathways abrogated the protective role of Yap overexpression on mitochondrial homeostasis and N2a cell survival in the setting of HR injury. Altogether, our data identified Yap as the endogenous defender to relieve HR-mediated nerve damage via antagonizing ROCK1/F-actin/mitochondrial fission pathways.

Indexed as

ActinsAdaptor Proteins, Signal TransducingAnimalsApoptosisHippo Signaling PathwayMiceMitochondriaMitochondrial DynamicsProtein Serine-Threonine KinasesReperfusion InjurySignal TransductionActinsAdaptor Proteins, Signal TransducingProtein Serine-Threonine KinasesApoptosisCerebral ischemia–reperfusion (IR) injuryMitochondrial fissionROCK1/F-actin pathways

Identifiers

PMID29796942
OpenAlexW2804907552

What OpenQuestion holds

Textmetadata
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.