ArticleCell & bioscience2024
WRN loss accelerates abnormal adipocyte metabolism in Werner syndrome.
Article in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Nicotinamide Riboside Supplementation Benefits in Patients With Werner Syndrome: A Double-Blind Randomized Crossover Placebo-Controlled Trial.Aging cell · 2025Trial
- Werner Syndrome Masquerading as Type 2 Diabetes: A Diagnostic Odyssey Leading to Precision Medicine.The American journal of case reports · 2026Article
- Deficiency of Werner RecQ-type DNA helicase causes premature malnutrition in zebrafish.iScience · 2026Article
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- The integration of WGCNA and ceRNA analysis provides insights into bovine intramuscular fat deposition.BMC genomics · 2025Article
- Emerging strategies, applications and challenges of targeting NADNature aging · 2025Review
- Review
- The mechanism of maternal inheritance of glycolipid metabolism disorder in a zebrafish model of type 2 diabetes.Scientific reports · 2025Article
- Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation.Aging · 2025Article
- Article
- Dietary restriction fails to extend lifespan of Drosophila model of Werner syndrome.G3 (Bethesda, Md.) · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundMetabolic dysfunction is one of the main symptoms of Werner syndrome (WS); however, the underlying mechanisms remain unclear. Here, we report that loss of WRN accelerates adipogenesis at an early stage both in vitro (stem cells) and in vivo (zebrafish). Moreover, WRN depletion causes a transient upregulation of late-stage of adipocyte-specific genes at an early stage.
methodsIn an in vivo study, we generated wrn
resultsOur findings show that mechanistically WRN deficiency causes SMARCA5 upregulation. SMARCA5 is crucial in chromatin remodeling and gene regulation. Additionally, rescuing WRN could normalize SMARCA5 expression and adipocyte differentiation. Moreover, we find that nicotinamide riboside (NR) supplementation restores adipocyte metabolism in both stem cells and zebrafish models.
conclusionsOur findings unravel a new mechanism for the influence of WRN in the early stage of adipogenesis and provide a possible treatment for metabolic dysfunction in WS. These data provide promising insights into potential therapeutics for ageing and ageing-related diseases.
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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.