Evidence map›Paper›PMID 36555780›Full record

ArticleInternational journal of molecular sciences2022

HIF-1α Causes LCMT1/PP2A Deficiency and Mediates Tau Hyperphosphorylation and Cognitive Dysfunction during Chronic Hypoxia.

Ling Lei, Jun Feng, Gang Wu, Zhen Wei, Jian-Zhi Wang, Bin Zhang, Rong Liu, Fei Liu, Xiaochuan Wang, Hong-Lian Li

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  4. Brain endothelial HIF-1Acta pharmaceutica Sinica. B · 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

10 authors at 4 institutions in 2 countries.

Ling LeiKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.
Jun FengDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Gang WuKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.
Zhen WeiKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.
Jian-Zhi WangKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.
Bin ZhangKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.
Rong LiuKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.ORCID 0000-0001-7477-6520
Fei LiuDepartment of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA.
Xiaochuan WangKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.ORCID 0000-0001-8207-0042
Hong-Lian LiKey Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.
Huazhong University of Science and Technology · CNNantong University · CNNew York State Office for People With Developmental Disabilities · USUnion Hospital · CN

Funding

National Natural Science Foundation of China 31929002National Natural Science Foundation of China 82071440National Natural Science Foundation of China 92049107
6 · The paper itself

Abstract

Chronic hypoxia is a risk factor for Alzheimer's disease (AD), and the neurofibrillary tangle (NFT) formed by hyperphosphorylated tau is one of the two major pathological changes in AD. However, the effect of chronic hypoxia on tau phosphorylation and its mechanism remains unclear. In this study, we investigated the role of HIF-1α (the functional subunit of hypoxia-inducible factor 1) in tau pathology. It was found that in Sprague-Dawley (SD) rats, global hypoxia (10% O

Indexed as

Alzheimer DiseaseCognitive DysfunctionHypoxia-Inducible Factor 1, alpha SubunitAnimalsHumansHypoxiaProtein Phosphatase 2RatsRats, Sprague-Dawleytau ProteinsHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitPpp2ca protein, ratProtein Phosphatase 2tau Proteinschronic hypoxiacognitive impairmentsHIF-1αleucine carboxyl methyltransferase 1protein phosphatase 2Atau

Identifiers

PMID36555780
PMCPMC9783654
OpenAlexW4312195155

What Socratic 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 Socratic graph.