ArticleAging cell2019
The p53/miRNAs/Ccna2 pathway serves as a novel regulator of cellular senescence: Complement of the canonical p53/p21 pathway.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 77 citations in OpenAlex.
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- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Lactate-related biomarkers in severe acute pancreatitis: insights from machine learning, molecular dynamics, and experimental validation.Journal of biological engineering · 2025Article
- Integrated mRNA-seq and miRNA-seq analysis reveals miR-210a-5p regulates uterine aging in laying hens by targeting the RASL11B/Raf/MAPK pathway.Journal of animal science and biotechnology · 2025Article
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- Connecting the Dots: How MicroRNAs Link Asthma and Atherosclerosis.International journal of molecular sciences · 2025Review
- AI-Driven Robotics Laboratory Identifies Pharmacological TNIK Inhibition as a Potent Senomorphic Agent.Aging and disease · 2025Article
- Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells.Cell reports. Medicine · 2024Article
- Article
- A hypothesis: MiRNA-124 mediated regulation of sirtuin 1 and vitamin D receptor gene expression accelerates aging.Aging medicine (Milton (N.S.W)) · 2024Article
- The Combined Anti-Aging Effect of Hydrolyzed Collagen Oligopeptides and Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells on Human Skin Fibroblasts.Molecules (Basel, Switzerland) · 2024Article
- Human Mesenchymal Stem Cell-Derived Exosomes Promote the Proliferation and Melanogenesis of Primary Melanocytes by Attenuating the HClinical, cosmetic and investigational dermatology · 2024Article
- Exploring senescence as a modifier of β cell extracellular vesicles in type 1 diabetes.Frontiers in endocrinology · 2024Review
- Exosomal miRNA-146a-5p Derived from Senescent Hepatocellular Carcinoma Cells Promotes Aging and Inhibits Aerobic Glycolysis in Liver Cells via Targeting IRF7.Journal of Cancer · 2024Article
- Amyloid-β Pathology-Specific Cytokine Secretion Suppresses Neuronal Mitochondrial Metabolism.Cellular and molecular bioengineering · 2023Article
- METTL3-mediated m6A modification of SIRT1 mRNA inhibits progression of endometriosis by cellular senescence enhancing.Journal of translational medicine · 2023Article
- Biochemical Targets and Molecular Mechanism of Matrine against Aging.International journal of molecular sciences · 2023Article
- Overexpression of adrenomedullin (ADM) alleviates the senescence of human dental pulp stem cells by regulating the miR-152/CCNA2 pathway.Cell cycle (Georgetown, Tex.) · 2023Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Aging is a multifactorial process characterized by the progressive deterioration of physiological functions. Among the multiple molecular mechanisms, microRNAs (miRNAs) have increasingly been implicated in the regulation of Aging process. However, the contribution of miRNAs to physiological Aging and the underlying mechanisms remain elusive. We herein performed high-throughput analysis using miRNA and mRNA microarray in the physiological Aging mouse, attempted to deepen into the understanding of the effects of miRNAs on Aging process at the "network" level. The data showed that various p53 responsive miRNAs, including miR-124, miR-34a and miR-29a/b/c, were up-regulated in Aging mouse compared with that in Young mouse. Further investigation unraveled that similar as miR-34a and miR-29, miR-124 significantly promoted cellular senescence. As expected, mRNA microarray and gene co-expression network analysis unveiled that the most down-regulated mRNAs were enriched in the regulatory pathways of cell proliferation. Fascinatingly, among these down-regulated mRNAs, Ccna2 stood out as a common target of several p53 responsive miRNAs (miR-124 and miR-29), which functioned as the antagonist of p21 in cell cycle regulation. Silencing of Ccna2 remarkably triggered the cellular senescence, while Ccna2 overexpression delayed cellular senescence and significantly reversed the senescence-induction effect of miR-124 and miR-29. Moreover, these p53 responsive miRNAs were significantly up-regulated during the senescence process of p21-deficient cells; overexpression of p53 responsive miRNAs or knockdown of Ccna2 evidently accelerated the cellular senescence in the absence of p21. Taken together, our data suggested that the p53/miRNAs/Ccna2 pathway might serve as a novel senescence modulator independent of p53/p21 pathway.
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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.