ArticleAging2015
Signaling pathway activation drift during aging: Hutchinson-Gilford Progeria Syndrome fibroblasts are comparable to normal middle-age and old-age cells.
Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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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.
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Who cites it
40 citing papers in PubMed, 71 citations in OpenAlex.
- Elevated SUN1 promotes migratory cell polarity defects through mechanically coupling microtubules to the nuclear lamina.Communications biology · 2025Article
- Precise progerin targeting using RfxCas13d: A therapeutic avenue for Hutchinson-Gilford progeria syndrome.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Maintenance of Chronological Aging Features in Culture of Normal Human Dermal Fibroblasts from Old Donors.Cells · 2022Article
- Progerin-expressing endothelial cells are unable to adapt to shear stress.Biophysical journal · 2022Article
- Is There an Interconnection between Epithelial-Mesenchymal Transition (EMT) and Telomere Shortening in Aging?International journal of molecular sciences · 2021Review
- Algorithmic Annotation of Functional Roles for Components of 3,044 Human Molecular Pathways.Frontiers in genetics · 2021Article
- The Resistance ofAntioxidants (Basel, Switzerland) · 2020Article
- Dietary magnesium supplementation improves lifespan in a mouse model of progeria.EMBO molecular medicine · 2020Article
- Peptide Hormone Regulation of DNA Damage Responses.Endocrine reviews · 2020Review
- Pharmacotherapy to gene editing: potential therapeutic approaches for Hutchinson-Gilford progeria syndrome.GeroScience · 2020Review
- Article
- Histone Acetyltransferase p300 Induces De Novo Super-Enhancers to Drive Cellular Senescence.Molecular cell · 2019Article
- New Insights into the Role of Epithelial⁻Mesenchymal Transition during Aging.International journal of molecular sciences · 2019Review
- Blood Biochemistry Analysis to Detect Smoking Status and Quantify Accelerated Aging in Smokers.Scientific reports · 2019Article
- Are There Common Mechanisms Between the Hutchinson-Gilford Progeria Syndrome and Natural Aging?Frontiers in genetics · 2019Review
- Expression of the Hutchinson-Gilford Progeria Mutation Leads to Aberrant Dentin Formation.Scientific reports · 2018Article
- Population Specific Biomarkers of Human Aging: A Big Data Study Using South Korean, Canadian, and Eastern European Patient Populations.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Inhibition of the acetyltransferase NAT10 normalizes progeric and aging cells by rebalancing the Transportin-1 nuclear import pathway.Science signaling · 2018Article
- Acquired resistance to tyrosine kinase inhibitors may be linked with the decreased sensitivity to X-ray irradiation.Oncotarget · 2018Article
- Protein sequestration at the nuclear periphery as a potential regulatory mechanism in premature aging.The Journal of cell biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For the past several decades, research in understanding the molecular basis of human aging has progressed significantly with the analysis of premature aging syndromes. Progerin, an altered form of lamin A, has been identified as the cause of premature aging in Hutchinson-Gilford Progeria Syndrome (HGPS), and may be a contributing causative factor in normal aging. However, the question of whether HGPS actually recapitulates the normal aging process at the cellular and organismal level, or simply mimics the aging phenotype is widely debated. In the present study we analyzed publicly available microarray datasets for fibroblasts undergoing cellular aging in culture, as well as fibroblasts derived from young, middle-age, and old-age individuals, and patients with HGPS. Using GeroScope pathway analysis and drug discovery platform we analyzed the activation states of 65 major cellular signaling pathways. Our analysis reveals that signaling pathway activation states in cells derived from chronologically young patients with HGPS strongly resemble cells taken from normal middle-aged and old individuals. This clearly indicates that HGPS may truly represent accelerated aging, rather than being just a simulacrum. Our data also points to potential pathways that could be targeted to develop drugs and drug combinations for both HGPS and normal aging.
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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.