ArticleThe EMBO journal2011
Aging and chronic DNA damage response activate a regulatory pathway involving miR-29 and p53.
Article in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
131 citing papers in PubMed, 1 synthesis or guideline pooled it, 255 citations in OpenAlex.
- Immunosenescence: A systems-level overview of immune cell biology and strategies for improving vaccine responses.Experimental gerontology · 2019Pooled it
- MicroRNA-29 acutely regulates memory stability, expression of synaptic genes, and DNA methylation in the mouse adult hippocampus.Cellular and molecular life sciences : CMLS · 2026Article
- Article
- Psmd13, a proteasome regulatory subunit identified in miR-29a regulation during neuronal differentiation.PloS one · 2026Article
- Article
- 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
- Regulatory Mechanisms of SPARC Overexpression in Melanoma Progression.International journal of molecular sciences · 2025Article
- Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson-Gilford Progeria Syndrome.Diseases (Basel, Switzerland) · 2025Article
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- miR-23a-mediated TRF2 repression in CD4 T cells from PLWH.Molecular immunology · 2025Article
- PP2C phosphatases-terminators of suicidal thoughts.Cell death & disease · 2024Review
- Negative feedback loop in the activation of non-homologous end joining DNA repair pathway in Helicobacter pylori infected patients with gastritis.Scientific reports · 2024Article
- miR-29 is an important driver of aging-related phenotypes.Communications biology · 2024Article
- Lowering Hippocampal miR-29a Expression Slows Cognitive Decline and Reduces Beta-Amyloid Deposition in 5×FAD Mice.Molecular neurobiology · 2024Article
- Noncoding RNA Contribution to Aging and Lifespan.The journals of gerontology. Series A, Biological sciences and medical sciences · 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
- Cellular senescence in skeletal disease: mechanisms and treatment.Cellular & molecular biology letters · 2023Review
- Aged mesenchymal stem cells and inflammation: from pathology to potential therapeutic strategies.Biology direct · 2023Review
- Progeria-a Rare Genetic Condition with Accelerated Ageing Process.Applied biochemistry and biotechnology · 2023Review
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a multifactorial process that affects most of the biological functions of the organism and increases susceptibility to disease and death. Recent studies with animal models of accelerated aging have unveiled some mechanisms that also operate in physiological aging. However, little is known about the role of microRNAs (miRNAs) in this process. To address this question, we have analysed miRNA levels in Zmpste24-deficient mice, a model of Hutchinson-Gilford progeria syndrome. We have found that expression of the miR-29 family of miRNAs is markedly upregulated in Zmpste24(-/-) progeroid mice as well as during normal aging in mouse. Functional analysis revealed that this transcriptional activation of miR-29 is triggered in response to DNA damage and occurs in a p53-dependent manner since p53(-/-) murine fibroblasts do not increase miR-29 expression upon doxorubicin treatment. We have also found that miR-29 represses Ppm1d phosphatase, which in turn enhances p53 activity. Based on these results, we propose the existence of a novel regulatory circuitry involving miR-29, Ppm1d and p53, which is activated in aging and in response to DNA damage.
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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.