ArticleMetabolic brain disease2022
Circ_0003611 regulates apoptosis and oxidative stress injury of Alzheimer's disease via miR-383-5p/KIF1B axis.
Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Cross-link Between CircRNAs and Neuroinflammation in Parkinson's Disease.Molecular neurobiology · 2026Review
- The emerging role of circular RNAs in neurodegenerative diseases and viral infections.Journal of neurovirology · 2026Review
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Unknotting the Role of circRNAs and IGF2BP3 in Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Emerging roles of circular RNAs and enhancer RNAs: new insights into the development and management of neurodegenerative disorders.Biomarker research · 2026Review
- The TRIM14-KIF1B Axis Drives Renal Injury in Diabetic Nephropathy Through TLR4/NF-κB Pathway Modulation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- MicroRNA-383-5p regulation of NADPH oxidase 4 alleviates hemorrhagic transformation and improves acute outcomes after endovascular recanalization in acute ischemic stroke.Frontiers in immunology · 2026Article
- The emerging role of circular RNAs in neuropsychiatric disorders.Translational psychiatry · 2025Review
- Regulation of Apoptotic Pathways by MicroRNAs: A Therapeutic Strategy for Alzheimer's Disease.Molecular neurobiology · 2025Review
- Emerging role and clinical applications of circular RNAs in human diseases.Functional & integrative genomics · 2025Review
- Exosomes and non-coding RNAs: bridging the gap in Alzheimer's pathogenesis and therapeutics.Metabolic brain disease · 2025Review
- The Role of circRNAs in the Pathological Mechanisms of Alzheimer's Disease: Potential Biomarkers for Diagnosis.Current neuropharmacology · 2025Review
- NcRNAs: A synergistically antiapoptosis therapeutic tool in Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- CircRNAs in Alzheimer's disease: What are the prospects?Non-coding RNA research · 2024Review
- The clinical perspective of circular RNAs in neurodegenerative diseases: potential diagnostic tools and therapeutic targets.Frontiers in cellular neuroscience · 2024Review
- miR-383-5p Regulates Preadipocyte Proliferation and Differentiation by TargetingInternational journal of molecular sciences · 2023Article
- Effect and mechanism of acupuncture on Alzheimer's disease: A review.Frontiers in aging neuroscience · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a high incidence neurodegenerative disease. Emerging evidence suggests that circular RNAs (circRNAs) play an important modulator in the pathogenesis of AD. The aim of this paper was to reconnoiter the effects of circular RNA_0003611 (circ_0003611) on Aβ-triggered neuronal injury in AD. In this work, the abundance of circ_0003611 was augmented in AD patients and SH-SY5Y and SK-N-SH cells treated with Aβ. Aβ-mediated cell proliferation, apoptosis, inflammatory response, oxidative stress, and glycolysis were abolished through circ_0003611 silencing. Circ_0003611 worked as a miR-383-5p sponge, and the protective role of circ_0003611 absence on Aβ-triggered neuronal injury was overturned by releasing miR-383-5p. Meanwhile, miR-383-5p directly targeted KIF1B, and miR-383-5p upregulation might relieve Aβ-triggered neuronal injury by reducing KIF1B expression. Mechanical analysis discovered that circ_0003611 served as a sponge of miR-383-5p to impact KIF1B expression. These findings indicated that circ_0003611 improved Aβ-triggered neuronal injury in AD through targeting the miR-383-5p/KIF1B axis, which might deliver innovative therapy targeting for AD.
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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.