ArticleStem cell reports2014
Telomerase protects werner syndrome lineage-specific stem cells from premature aging.
Article in Stem cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 100 citations in OpenAlex.
- Review
- Preventing MSC aging and enhancing immunomodulation: Novel strategies for cell-based therapies.Regenerative therapy · 2025Review
- SOX9 haploinsufficiency reveals SOX9-Noggin interaction in BMP-SMAD signaling pathway in chondrogenesis.Cellular and molecular life sciences : CMLS · 2025Article
- Amelioration of premature aging in Werner syndrome stem cells by targeting SHIP/AKT pathway.Cell & bioscience · 2025Article
- A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches.Cancers · 2025Review
- Strategies for modeling aging and age-related diseases.npj aging · 2024Review
- Differential Gene Expression followingInternational journal of molecular sciences · 2024Article
- Werner Syndrome Caused by Homozygous Frameshift Variant c.1578del inActa medica Lituanic · 2024Article
- RNaseH2A downregulation drives inflammatory gene expression via genomic DNA fragmentation in senescent and cancer cells.Communications biology · 2022Article
- High-confidence cancer patient stratification through multiomics investigation of DNA repair disorders.Cell death & disease · 2022Article
- Review
- Aging of mesenchymal stem cell: machinery, markers, and strategies of fighting.Cellular & molecular biology letters · 2022Review
- Developing Bottom-Up Induced Pluripotent Stem Cell Derived Solid Tumor Models Using Precision Genome Editing Technologies.The CRISPR journal · 2022Review
- APOE4 exacerbates α-synuclein seeding activity and contributes to neurotoxicity in Alzheimer's disease with Lewy body pathology.Acta neuropathologica · 2022Article
- Mesenchymal Stem/Stromal Cell Senescence: Hallmarks, Mechanisms, and Combating Strategies.Stem cells translational medicine · 2022Review
- Cerebroprotein hydrolysate-I protects senescence-induced by D-galactose in PC12 cells and mice.Food science & nutrition · 2021Article
- Review
- Reprogramming: Emerging Strategies to Rejuvenate Aging Cells and Tissues.International journal of molecular sciences · 2021Review
- Telomerase expression marks transitional growth-associated skeletal progenitor/stem cells.Stem cells (Dayton, Ohio) · 2021Article
- Crosstalk among DNA Damage, Mitochondrial Dysfunction, Impaired Mitophagy, Stem Cell Attrition, and Senescence in the Accelerated Ageing Disorder Werner Syndrome.Cytogenetic and genome research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Werner syndrome (WS) patients exhibit premature aging predominantly in mesenchyme-derived tissues, but not in neural lineages, a consequence of telomere dysfunction and accelerated senescence. The cause of this lineage-specific aging remains unknown. Here, we document that reprogramming of WS fibroblasts to pluripotency elongated telomere length and prevented telomere dysfunction. To obtain mechanistic insight into the origin of tissue-specific aging, we differentiated iPSCs to mesenchymal stem cells (MSCs) and neural stem/progenitor cells (NPCs). We observed recurrence of premature senescence associated with accelerated telomere attrition and defective synthesis of the lagging strand telomeres in MSCs, but not in NPCs. We postulate this "aging" discrepancy is regulated by telomerase. Expression of hTERT or p53 knockdown ameliorated the accelerated aging phenotypein MSC, whereas inhibition of telomerase sensitized NPCs to DNA damage. Our findings unveil a role for telomerase in the protection of accelerated aging in a specific lineage of stem cells.
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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.