Evidence map›Paper›PMID 31551758›Full record

ArticleFrontiers in aging neuroscience2019

Appoptosin Mediates Lesions Induced by Oxidative Stress Through the JNK-FoxO1 Pathway.

Cuilin Zhang, Zhenqiu Tan, Yongzhuang Xie, Yingjun Zhao, Timothy Y Huang, Zhaoping Lu, Hong Luo, Dan Can, Huaxi Xu, Yun-Wu Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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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

11 authors at 4 institutions in 2 countries.

Cuilin ZhangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Zhenqiu TanFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Yongzhuang XieFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Yingjun ZhaoFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Timothy Y HuangNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, United States.
Zhaoping LuFujian Provincial Maternity and Children's Hospital of Fujian Medical University, Fuzhou, China.
Hong LuoFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Dan CanFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Huaxi XuNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, United States.
Yun-Wu ZhangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Xian ZhangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, School of Medicine, Institute of Neuroscience, Xiamen University, Xiamen, China.
Xiamen University · CNDiscovery Institute · USFujian Medical University · CNSanford Burnham Prebys Medical Discovery Institute · US

Funding

Novel roles for the Alzheimer's Disease (AD) risk gene, SORLA in neuroprotection in ADR01AG061875 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HUANG, TIMOTHY YIKAI · 2018 to 2022
$3.4M
A role for TREM2/Abeta interactions in microglia-regulated AD pathogenesisR21AG059217 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HUANG, TIMOTHY YIKAI · 2018 to 2019
$536k
NIA NIH HHS R01 AG061875NIA NIH HHS R21 AG059217
6 · The paper itself

Abstract

Oxidative stress is a common feature of neurodegenerative diseases and plays an important role in disease progression. Appoptosin is a pro-apoptotic protein that contributes to the pathogenesis of neurodegenerative diseases such as Alzheimer's disease and progressive supranuclear palsy. However, whether appoptosin mediates oxidative stress-induced neurotoxicity has yet to be determined. Here, we observe that appoptosin protein levels are induced by hydrogen peroxide (H

Indexed as

appoptosinFoxO1JNKoxidative stressROS

Identifiers

PMID31551758
PMCPMC6737070
OpenAlexW2969406449

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.