ArticleAging2012
Down regulation of miR-124 in both Werner syndrome DNA helicase mutant mice and mutant Caenorhabditis elegans wrn-1 reveals the importance of this microRNA in accelerated aging.
Article in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Dietary restriction fails to extend lifespan of Drosophila model of Werner syndrome.G3 (Bethesda, Md.) · 2024Article
- Characterization of Stress Responses in aBiomolecules · 2021Article
- Review
- Antioxidant and Anti-Inflammaging Ability of Prune (Antioxidants (Basel, Switzerland) · 2021Article
- Article
- The p53/miRNAs/Ccna2 pathway serves as a novel regulator of cellular senescence: Complement of the canonical p53/p21 pathway.Aging cell · 2019Article
- MicroRNAs in hereditary and sporadic premature aging syndromes and other laminopathies.Aging cell · 2018Review
- Single-molecule studies reveal reciprocating of WRN helicase core along ssDNA during DNA unwinding.Scientific reports · 2017Article
- Elucidating the Mechanism of Weissella-dependent Lifespan Extension in Caenorhabditis elegans.Scientific reports · 2015Article
- Effects of nutritional components on aging.Aging cell · 2015Review
- Profiling age-related epigenetic markers of stomach adenocarcinoma in young and old subjects.Cancer informatics · 2015Article
- Expression profile of Caenorhabditis elegans mutant for the Werner syndrome gene ortholog reveals the impact of vitamin C on development to increase life span.BMC genomics · 2014Article
- Effect of aging on microRNAs and regulation of pathogen recognition receptors.Current opinion in immunology · 2014Review
- Identification of microRNAs dysregulated in cellular senescence driven by endogenous genotoxic stress.Aging · 2013Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Small non-coding microRNAs are believed to be involved in the mechanism of aging but nothing is known on the impact of microRNAs in the progeroid disorder Werner syndrome (WS). WS is a premature aging disorder caused by mutations in a RecQ-like DNA helicase. Mice lacking the helicase domain of the WRN ortholog exhibit many phenotypic features of WS, including a pro-oxidant status and a shorter mean life span.Caenorhabditis elegans (C. elegans) with a nonfunctional wrn-1 DNA helicase also exhibit a shorter life span. Thus, both models are relevant to study the expression of microRNAs involved in WS. In this study, we show that miR-124 expression is lost in the liver of Wrn helicase mutant mice. Interestingly, the expression of this conserved miR-124 in whole wrn-1 mutant worms is also significantly reduced. The loss of mir-124 in C. elegans increases reactive oxygen species formation and accumulation of the aging marker lipofuscin, reduces whole body ATP levels and results in a reduction in life span. Finally, supplementation of vitamin C normalizes the median life span of wrn-1 and mir-124 mutant worms. These results suggest that biological pathways involving WRN and miR-124 are conserved in the aging process across different species.
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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.