Evidence map›Paper›PMID 24988431›Full record

ArticleAutophagy2014

ARRB1/β-arrestin-1 mediates neuroprotection through coordination of BECN1-dependent autophagy in cerebral ischemia.

Pei Wang, Tian-Ying Xu, Kai Wei, Yun-Feng Guan, Xia Wang, Hui Xu, Ding-Feng Su, Gang Pei, Chao-Yu Miao

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 2 pooled it
9.2field-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, 2 syntheses or guidelines pooled it, 132 citations in OpenAlex.

  1. Guideline
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  5. Acetate enhances neuronal plasticity and reduces ischemic brain injury by promoting tau protein lactylation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Article
  6. Review
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  14. Article
  15. Review
  16. Article
  17. The landscape of meLife · 2023
    Article
  18. Article
  19. Article
  20. Article

30 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Pei WangDepartment of Pharmacology; Second Military Medical University; Shanghai, China.
Tian-Ying XuDepartment of Pharmacology; Second Military Medical University; Shanghai, China.
Kai WeiDepartment of Pharmacology; Second Military Medical University; Shanghai, China.
Yun-Feng GuanDepartment of Pharmacology; Second Military Medical University; Shanghai, China.
Xia WangDepartment of Pharmacology; Second Military Medical University; Shanghai, China.
Hui XuInstitute of Biochemistry and Cell Biology; Shanghai Institutes for Biological Sciences; Chinese Academy of Sciences; Shanghai, China.
Ding-Feng SuDepartment of Pharmacology; Second Military Medical University; Shanghai, China.
Gang PeiInstitute of Biochemistry and Cell Biology; Shanghai Institutes for Biological Sciences; Chinese Academy of Sciences; Shanghai, China; School of Life Science and Technology; Tongji University; Shanghai, China.
Chao-Yu MiaoDepartment of Pharmacology; Second Military Medical University; Shanghai, China; Center of Stroke; Beijing Institute for Brain Disorders; Beijing, China.
Second Military Medical University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, a highly conserved process conferring cytoprotection against stress, contributes to the progression of cerebral ischemia. β-arrestins are multifunctional proteins that mediate receptor desensitization and serve as important signaling scaffolds involved in numerous physiopathological processes. Here, we show that both ARRB1 (arrestin, β 1) and ARRB2 (arrestin, β 2) were upregulated by cerebral ischemic stress. Knockout of Arrb1, but not Arrb2, aggravated the mortality, brain infarction, and neurological deficit in a mouse model of cerebral ischemia. Accordingly, Arrb1-deficient neurons exhibited enhanced cell injury upon oxygen-glucose deprivation (OGD), an in vitro model of ischemia. Deletion of Arrb1 did not affect the cerebral ischemia-induced inflammation, oxidative stress, and nicotinamide phosphoribosyltransferase upregulation, but markedly suppressed autophagy and induced neuronal apoptosis/necrosis in vivo and in vitro. Additionally, we found that ARRB1 interacted with BECN1/Beclin 1 and PIK3C3/Vps34, 2 major components of the BECN1 autophagic core complex, under the OGD condition but not normal conditions in neurons. Finally, deletion of Arrb1 impaired the interaction between BECN1 and PIK3C3, which is a critical event for autophagosome formation upon ischemic stress, and markedly reduced the kinase activity of PIK3C3. These findings reveal a neuroprotective role for ARRB1, in the context of cerebral ischemia, centered on the regulation of BECN1-dependent autophagosome formation.

Indexed as

AnimalsApoptosis Regulatory ProteinsArrestinsAutophagyBeclin-1beta-Arrestin 1beta-Arrestin 2beta-ArrestinsBrain IschemiaCells, CulturedDisease Models, AnimalMaleMiceMice, KnockoutNeuronsSignal TransductionApoptosis Regulatory ProteinsArrb1 protein, mouseArrb2 protein, mouseArrestinsBeclin-1Becn1 protein, mousebeta-Arrestin 1beta-Arrestin 2beta-ArrestinsARRB1autophagyBECN1cerebral ischemianeuron

Identifiers

PMID24988431
PMCPMC4206533
OpenAlexW1989745622

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.