Evidence map›Paper›PMID 30014904›Full record

ArticleRedox biology2018

Breast cancer susceptibility protein 1 (BRCA1) rescues neurons from cerebral ischemia/reperfusion injury through NRF2-mediated antioxidant pathway.

Pengfei Xu, Qian Liu, Yi Xie, Xiaolei Shi, Yunzi Li, Mengna Peng, Hongquan Guo, Rui Sun, Juanji Li, Ye Hong and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. 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 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 109 citations in OpenAlex.

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  18. Roles of NRF2 in DNA damage repair.Cellular oncology (Dordrecht, Netherlands) · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Pengfei XuDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Qian LiuDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Yi XieDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Xiaolei ShiKinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia, Canada; Department of Neurology, The First Affiliated Hospital, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui 241001, China.
Yunzi LiDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Mengna PengDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Hongquan GuoDepartment of Neurology, Jinling Hospital, Southern Medical University, Nanjing, Jiangsu 210002, China.
Rui SunDepartment of Neurology, Jinling Clinical College of Nanjing Medical University, Nanjing, Jiangsu 210002, China.
Juanji LiDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Ye HongDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Xinfeng LiuDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China. Electronic address: xfliu2@vip.163.com.
Gelin XuDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002, China. Electronic address: gelinxu@nju.edu.cn.
Nanjing General Hospital of Nanjing Military Command · CNNanjing Medical University · CNUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular oxidative stress plays a vital role in the pathological process of neural damage in cerebral ischemia/reperfusion (I/R). The breast cancer susceptibility protein 1 (BRCA1), a tumor suppressor, can modulate cellular antioxidant response and DNA repair. Yet the role of BRCA1 in cerebral I/R injury has not been explored. In this study, we observed that BRCA1 was mainly expressed in neurons and was up-regulated in response to I/R insult. Overexpression of BRCA1 attenuated reactive oxygen species production and lipid peroxidation. Enhanced BRCA1 expression promoted DNA double strand break repair through non-homologous end joining pathway. These effects consequently led to neuronal cell survival and neurological recovery. Mechanically, BRCA1 can interact with the nuclear factor (erythroid-derived 2)-like 2 (NRF2) through BRCA1 C-terminal (BRCT) domain. The cross-talk between BRCT and NRF2 activated the NRF2/Antioxidant Response Element signaling pathway and thus protected injured neurons during cerebral I/R. In conclusion, enhanced BRCA1 after cerebral I/R injury may attenuate or prevent neural damage from I/R via NRF2-mediated antioxidant pathway. The finding may provide a potential therapeutic target against ischemic stroke.

Indexed as

Oxidative StressSignal TransductionAnimalsAntioxidant Response ElementsApoptosisBrain IschemiaBRCA1 ProteinMaleMice, Inbred C57BLNeuronsNF-E2-Related Factor 2Reperfusion InjuryTumor Suppressor ProteinsBRCA1 ProteinBrca1 protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2Tumor Suppressor ProteinsBRCA1DNA damageIschemia/ReperfusionNRF2Oxidative stress

Identifiers

PMID30014904
PMCPMC6068089
OpenAlexW2832629985

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.