Evidence map›Paper›PMID 32627121›Full record

ArticleJournal of molecular neuroscience : MN2021

Anti-aging Klotho Protects SH-SY5Y Cells Against Amyloid β1-42 Neurotoxicity: Involvement of Wnt1/pCREB/Nrf2/HO-1 Signaling.

Mohsen Sedighi, Tourandokht Baluchnejadmojarad, Siamak Afshin-Majd, Mona Amiri, Malihe Aminzade, Mehrdad Roghani

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Article in Journal of molecular neuroscience : MN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  6. Rationally Designed Peptoid Inhibitors of Amyloid-β Oligomerization.Chembiochem : a European journal of chemical biology · 2024
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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

6 authors at 3 institutions in 1 country.

Mohsen SedighiDepartment of Neuroscience, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0003-0608-7840
Tourandokht BaluchnejadmojaradDepartment of Neuroscience, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran. Baluchnejadmojarad.t@iums.ac.ir.
Siamak Afshin-MajdNeurophysiology Research Center, Shahed University, Tehran, Iran.
Mona AmiriDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Malihe AminzadeInstitute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran.
Mehrdad RoghaniNeurophysiology Research Center, Shahed University, Tehran, Iran.
Iran University of Medical Sciences · IRShahed University · IRUniversity of Tehran · IR

Funding

Iran University of Medical Sciences grant # 95-01-87-27994
6 · The paper itself

Abstract

Alzheimer's disease (AD) is considered a prevalent neurological disorder with a neurodegenerative nature in elderly people. Oxidative stress and neuroinflammation due to amyloid β (Aβ) peptides are strongly involved in AD pathogenesis. Klotho is an anti-aging protein with multiple protective effects that its deficiency is involved in development of age-related disorders. In this study, we investigated the beneficial effect of Klotho pretreatment at different concentrations of 0.5, 1, and 2 nM against Aβ1-42 toxicity at a concentration of 20 μM in human SH-SY5Y neuroblastoma cells. Our findings showed that Klotho could significantly and partially restore cell viability and decrease reactive oxygen species (known as ROS) and improve superoxide dismutase activity (SOD) in addition to reduction of caspase 3 activity and DNA fragmentation following Aβ1-42 challenge. In addition, exogenous Klotho also reduced inflammatory biomarkers consisting of nuclear factor-kB (NF-kB), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in Aβ-exposed cells. Besides, Klotho caused downregulation of Wnt1 level, upregulation of phosphorylated cyclic AMP response element binding (pCREB), and mRNA levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) with no significant alteration of epsilon isoform of protein kinase C (PKCε) after Aβ toxicity. In summary, Klotho could alleviate apoptosis, oxidative stress, and inflammation in human neuroblastoma cells after Aβ challenge and its beneficial effect is partially exerted through appropriate modulation of Wnt1/pCREB/Nrf2/HO-1 signaling.

Indexed as

Amyloid beta-PeptidesApoptosisCell Line, TumorCellular SenescenceCREB-Binding ProteinDNA FragmentationGlucuronidaseHeme Oxygenase-1HumansInflammationKlotho ProteinsNeuroblastomaNF-E2-Related Factor 2Oxidative StressPeptide FragmentsReactive Oxygen SpeciesAmyloid beta-Peptidesamyloid beta-protein (1-42)CREB-Binding ProteinGlucuronidaseHeme Oxygenase-1HMOX1 protein, humanKlotho ProteinsNFE2L2 protein, humanNF-E2-Related Factor 2Peptide FragmentsReactive Oxygen SpeciesRecombinant ProteinsSuperoxide DismutaseWnt1 ProteinWNT1 protein, humanAlzheimer diseaseAmyloid beta-proteinApoptosisKlotho proteinOxidative stress

Identifiers

PMID32627121
OpenAlexW3038778274

What OpenQuestion holds

Textmetadata
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.