Evidence map›Paper›PMID 31430865›Full record

ArticleCells2019

17β-Estradiol Modulates SIRT1 and Halts Oxidative Stress-Mediated Cognitive Impairment in a Male Aging Mouse Model.

Mehtab Khan, Rahat Ullah, Shafiq Ur Rehman, Shahid Ali Shah, Kamran Saeed, Tahir Muhammad, Hyun Young Park, Myeung Hoon Jo, Kyonghwan Choe, Bart P F Rutten and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.9field-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

53 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  7. Effect of Estrogen on Sirt1 Signaling in Human Macrophages.International journal of molecular sciences · 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

11 authors at 2 institutions in 2 countries.

Mehtab KhanDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.
Rahat UllahDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.
Shafiq Ur RehmanDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.
Shahid Ali ShahDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.
Kamran SaeedDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.
Tahir MuhammadDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.ORCID 0000-0001-5819-1397
Hyun Young ParkDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Medical Center (MUMC+), Faculty of Health, Medicine and Life Sciences, Maastricht University, European Graduate School of Neuroscience (EURON), 6229ER Maastricht, The Netherlands.
Myeung Hoon JoDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.
Kyonghwan ChoeDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Medical Center (MUMC+), Faculty of Health, Medicine and Life Sciences, Maastricht University, European Graduate School of Neuroscience (EURON), 6229ER Maastricht, The Netherlands.
Bart P F RuttenDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Medical Center (MUMC+), Faculty of Health, Medicine and Life Sciences, Maastricht University, European Graduate School of Neuroscience (EURON), 6229ER Maastricht, The Netherlands.ORCID 0000-0002-9834-6346
Myeong Ok KimDivision of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea. mokim@gnu.ac.kr.
Gyeongsang National University · KRMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress has been considered the main mediator in neurodegenerative disease and in normal aging processes. Several studies have reported that the accumulation of reactive oxygen species (ROS), elevated oxidative stress, and neuroinflammation result in cellular malfunction. These conditions lead to neuronal cell death in aging-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease. Chronic administration of d-galactose (d-gal) for a period of 10 weeks causes ROS generation and neuroinflammation, ultimately leading to cognitive impairment. In this study, we evaluated the estrogen receptor α (ERα)/silent mating type information regulation 2 homolog 1 (SIRT1)-dependent antioxidant efficacy of 17β-estradiol against d-gal-induced oxidative damage-mediated cognitive dysfunction in a male mouse model. The results indicate that 17β-estradiol, by stimulating ERα/SIRT1, halts d-gal-induced oxidative stress-mediated JNK/NF-ҡB overexpression, neuroinflammation and neuronal apoptosis. Moreover, 17β-estradiol ameliorated d-gal-induced AD-like pathophysiology, synaptic dysfunction and memory impairment in adult mouse brains. Interestingly, inhibition of SIRT1 with Ex527 (a potent and selective SIRT1 inhibitor) further enhanced d-gal-induced toxicity and abolished the beneficial effect of 17β-estradiol. Most importantly, for the first time, our molecular docking study reveals that 17β-estradiol allosterically increases the expression of SIRT1 and abolishes the inhibitory potential of d-ga. In summary, we can conclude that 17β-estradiol, in an ERα/SIRT1-dependent manner, abrogates d-gal-induced oxidative stress-mediated memory impairment, neuroinflammation, and neurodegeneration in adult mice.

Indexed as

AnimalsCell Line, TumorCognitive DysfunctionDisease Models, AnimalEstradiolGalactoseMaleMiceMice, Inbred C57BLNeurodegenerative DiseasesOxidative StressReactive Oxygen SpeciesReceptors, EstradiolSirtuin 1EstradiolGalactoseReactive Oxygen SpeciesReceptors, EstradiolSirt1 protein, mouseSirtuin 117β-Estradiold-galactoseneuroinflammation neurodegenerationROSSIRT1

Identifiers

PMID31430865
PMCPMC6721687
OpenAlexW2968592185

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.