ArticleMolecular neurobiology2023
CircLPAR1 Promotes Neuroinflammation and Oxidative Stress in APP/PS1 Mice by Inhibiting SIRT1/Nrf-2/HO-1 Axis Through Destabilizing GDF-15 mRNA.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- A systematic review of the neuroprotective role and biomarker potential of GDF15 in neurodegeneration.Frontiers in immunology · 2024Pooled it
- UPF1 promotes wound healing in diabetic foot ulcer by reducing CYP1A1-induced oxidative stress through enhancing EGR1 degradation.Molecular genetics and genomics : MGG · 2026Article
- Pharmacological Blockade of LPAR1 Does Not Provide Neuroprotection in a Rat Model of Ocular Hypertensive Glaucoma.Translational vision science & technology · 2026Article
- CircRNA-Based Therapeutics: a New Frontier in Neuroinflammation Treatment.Molecular neurobiology · 2025Review
- The emerging role of circular RNAs in neuropsychiatric disorders.Translational psychiatry · 2025Review
- Delphinidin attenuates cognitive deficits and pathology of Alzheimer's disease by preventing microglial senescence via AMPK/SIRT1 pathway.Alzheimer's research & therapy · 2025Article
- 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
- Diversity of Microglia-Derived Molecules with Neurotrophic Properties That Support Neurons in the Central Nervous System and Other Tissues.Molecules (Basel, Switzerland) · 2024Review
- CircMAPK1 induces cell pyroptosis in sepsis-induced lung injury by mediating KDM2B mRNA decay to epigenetically regulate WNK1.Molecular medicine (Cambridge, Mass.) · 2024Article
- GDF15 induces chemoresistance to oxaliplatin by forming a reciprocal feedback loop with Nrf2 to maintain redox homeostasis in colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Network analysis-guided drug repurposing strategies targeting LPAR receptor in the interplay of COVID, Alzheimer's, and diabetes.Scientific reports · 2024Article
- N6-methyladenosine-modified circRIMS2 mediates synaptic and memory impairments by activating GluN2B ubiquitination in Alzheimer's disease.Translational neurodegeneration · 2023Article
- Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration.Journal of biomedical science · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Circular RNA LPAR1 (circLPAR1) was revealed to be elevated in Alzheimer's disease (AD); nevertheless, its role and mechanisms in AD remain unknown. Memory performance of APP/PS1 mice was assessed by Morris water maze test. Expression of circLPAR1 and indicated messenger RNA (mRNA) in mouse brain tissues or/and SH-SY5Y cells were tested by quantitative real-time PCR (qRT-PCR). Protein expression of indicated gene was examined by western blot. Production of proinflammatory cytokines (tumor necrosis factor-α, TNF-α; interleukin-6, IL-6; interleukin-1β, IL-1β; and interleukin-8, IL-8) and oxidative stress-related factors (reactive oxygen species, ROS; malondialdehyde, MDA; superoxide dismutase, SOD; and glutathione, GSH) were assessed by commercial kits. RNA pull down and RNA immunoprecipitation were performed to verify the interplay between up-frameshift protein 1 (UPF1) and circLPAR1 or growth differentiation factor 15 (GDF-15). CircLPAR1 was elevated, while GDF-15 was decreased in both APP/PS1 mice and Aβ-treated SH-SY5Y cells. Knockdown of circLPAR1 and overexpression of GDF-15 protected cells against Aβ-caused inflammation, oxidative stress, and neuronal apoptosis. CircLPAR1 knockdown was also proved to improve AD-related pathological traits and ameliorate cognitive dysfunctions in vivo. In mechanism, we found that circLPAR1 repressed GDF-15 expression by decreasing GDF-15 mRNA stability through UPF1 recruitment. Rescue assays suggested that sirtuin 1 (SIRT1) knockdown reversed GDF-15 overexpression-induced inhibition on Aβ-induced neuronal damage and nuclear factor E2-related factor (Nrf-2)/heme oxygenase-1 (HO-1) pathway inhibition. Moreover, the protective effect of circLPAR1 knockdown against Aβ-induced apoptosis was abolished by GDF-15 knockdown, and SIRT1 overexpression could counteract this effect of GDF-15 knockdown. CircLPAR1 knockdown improved AD-related pathological traits in vitro and in vivo by inhibiting SIRT1/Nrf-2/HO-1 axis through GDF-15.
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