ArticleCell death & disease2020
ZNF746/PARIS overexpression induces cellular senescence through FoxO1/p21 axis activation in myoblasts.
Article in Cell death & disease, 2020. 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, 22 citations in OpenAlex.
- Meloxicam protects against muscle and metabolic decline in ageing through Cdon restoration and oxidative stress modulation.Experimental & molecular medicine · 2026Article
- FOXO family and neurodegenerative diseases: Mechanisms of action and therapeutic potential.Redox biology · 2026Review
- Engineered Clostridium butyricum-pMTL007-GLP-1 Delays Neurodegeneration in Prnp-SNCA*A53T Transgenic Mice Model by Suppressing Astrocyte Senescence.Probiotics and antimicrobial proteins · 2026Article
- SKP2 in Cancer: From Molecular Regulation to Therapeutic Vulnerabilities and Translational Perspectives.Drug design, development and therapy · 2026Review
- Panaxatriol exerts anti-senescence effects and alleviates osteoarthritis and cartilage repair fibrosis by targeting UFL1.Journal of advanced research · 2025Article
- Perspectives on mitochondrial dysfunction in the regeneration of aging skeletal muscle.Cellular & molecular biology letters · 2025Review
- FOXO1 contributes to cigarette smoke condensate-induced cellular senescence and fibrosis in lung fibroblasts through activating the TGF-β1/Smad2/3 signaling pathway.Immunologic research · 2025Article
- The Extract ofInternational journal of molecular sciences · 2024Article
- Proximity proteomic analysis of the NRF family reveals the Parkinson's disease protein ZNF746/PARIS as a co-complexed repressor of NRF2.Science signaling · 2023Article
- The roles of miRNAs in adult skeletal muscle satellite cells.Free radical biology & medicine · 2023Review
- Chiisanoside Mediates the Parkin/ZNF746/PGC-1α Axis by Downregulating MiR-181a to Improve Mitochondrial Biogenesis in 6-OHDA-Caused Neurotoxicity Models In Vitro and In Vivo: Suggestions for Prevention of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Article
- Automatic Text-Mining Approach to Identify Molecular Target Candidates Associated with Metabolic Processes for Myotonic Dystrophy Type 1.International journal of environmental research and public health · 2023Article
- Plasma Metabolomics and Machine Learning-Driven Novel Diagnostic Signature for Non-Alcoholic Steatohepatitis.Biomedicines · 2022Article
- A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Article
- Waiting for PARIS-A Biological Target in Search of a Drug.Journal of Parkinson's disease · 2022Article
- Parkin interacting substrate phosphorylation by c-Abl drives dopaminergic neurodegeneration.Brain : a journal of neurology · 2021Article
- Concentration Dependence of the Antioxidant and Prooxidant Activity of Trolox in HeLa Cells: Involvement in the Induction of Apoptotic Volume Decrease.Antioxidants (Basel, Switzerland) · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various stresses, including oxidative stress, impair the proliferative capacity of muscle stem cells leading to declined muscle regeneration related to aging or muscle diseases. ZNF746 (PARIS) is originally identified as a substrate of E3 ligase Parkin and its accumulation is associated with Parkinson's disease. In this study, we investigated the role of PARIS in myoblast function. PARIS is expressed in myoblasts and decreased during differentiation. PARIS overexpression decreased both proliferation and differentiation of myoblasts without inducing cell death, whereas PARIS depletion enhanced myoblast differentiation. Interestingly, high levels of PARIS in myoblasts or fibroblasts induced cellular senescence with alterations in gene expression associated with p53 signaling, inflammation, and response to oxidative stress. PARIS overexpression in myoblasts starkly enhanced oxidative stress and the treatment of an antioxidant Trolox attenuated the impaired proliferation caused by PARIS overexpression. FoxO1 and p53 proteins are elevated in PARIS-overexpressing cells leading to p21 induction and the depletion of FoxO1 or p53 reduced p21 levels induced by PARIS overexpression. Furthermore, both PARIS and FoxO1 were recruited to p21 promoter region and Trolox treatment attenuated FoxO1 recruitment. Taken together, PARIS upregulation causes oxidative stress-related FoxO1 and p53 activation leading to p21 induction and cellular senescence of myoblasts.
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