ArticleJournal of molecular neuroscience : MN2020
MicroRNA-107 Ameliorates Damage in a Cell Model of Alzheimer's Disease by Mediating the FGF7/FGFR2/PI3K/Akt Pathway.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Fibroblast growth factors in Alzheimer's Disease pathogenesis: neuropharmacological implications for neuroprotection, neurogenesis, and therapeutic development.Molecular biology reports · 2026Review
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- FGFs/FGFRs and neuroinflammatory diseases: mechanism, drug therapies and delivery systems.Journal of advanced research · 2025Review
- Denoising self-supervised learning for disease-gene association prediction.BMC bioinformatics · 2025Article
- Regulation of Apoptotic Pathways by MicroRNAs: A Therapeutic Strategy for Alzheimer's Disease.Molecular neurobiology · 2025Review
- Coenzyme Q10 alleviates AlClToxicology research · 2025Article
- Untangling the Genetic Threads of Alzheimer's: Insights into Risk Factors and Biomarkers.Current gene therapy · 2025Review
- Insights into the Role of microRNAs as Clinical Tools for Diagnosis, Prognosis, and as Therapeutic Targets in Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Non-Coding RNAs and Neurodegenerative Diseases: Information of their Roles in Apoptosis.Molecular neurobiology · 2024Review
- Exploring the Regulatory Landscape of Dementia: Insights from Non-Coding RNAs.International journal of molecular sciences · 2024Review
- NcRNAs: A synergistically antiapoptosis therapeutic tool in Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- miR-107-5p ameliorates neurological damage, oxidative stress, and immune responses in mice with Alzheimer's disease by suppressing the Toll-like receptor 4 (TLR4)/nuclear factor-kappaB(NF-κB) pathway.The Kaohsiung journal of medical sciences · 2024Article
- Article
- Mechanism and Therapeutic Prospect of miRNAs in Neurodegenerative Diseases.Behavioural neurology · 2023Review
- Circ_0049472 regulates the damage of Aβ-induced SK-N-SH and CHP-212 cells by mediating the miR-107/KIF1B axis.Experimental brain research · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- MicroRNA Alteration, Application as Biomarkers, and Therapeutic Approaches in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Alzheimer's Disease: An Update and Insights Into Pathophysiology.Frontiers in aging neuroscience · 2022Review
- Article
- Non-coding RNAs and their bioengineering applications for neurological diseases.Bioengineered · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD), the most prevalent representation of dementia, is a neurodegenerative disease resulting from the degenerative disturbance of the central nervous system. Previous studies have indicated that miR-107 is reduced in the brain neocortex of patients with AD; however, its underlying mechanism is not clear. Therefore, the objective of this study was to explore the question of whether miR-107 participates in AD development. The study confirmed that the miR-107 expression levels were dramatically decreased in patients with AD and in beta-amyloid (Aβ) (Aβ)-treated SH-SY5Y cells compared with control groups. Upregulation of miR-107 reversed the inhibitory role of Aβ on cell proliferation and viability. In addition, miR-107 upregulation also ameliorated the Aβ-induced inflammation and apoptosis of SH-SY5Y cells. Furthermore, using bioinformatic prediction, dual-luciferase reporter assay (DLRA), quantitative polymerase chain reaction (qPCR), and Western blot (WB), miR-107 was confirmed to reduce the expression level of FGF7, and it subsequently deactivated the FGFR2/PI3K/Akt pathway. Moreover, FGF7 overexpression counteracted the role of miR-107 in the viability, proliferation, inflammation, and apoptosis of Aβ-induced SH-SY5Y cells.
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What OpenQuestion holds
Registered trials
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.