ArticleAging cell2017
Reprogramming progeria fibroblasts re-establishes a normal epigenetic landscape.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Organ-Specific Dedifferentiation and Epigenetic Remodeling in In Vivo Reprogramming.Aging cell · 2025Review
- Article
- Generation of Nonintegrative-Induced Pluripotent Stem Cells in Hutchinson-Gilford Progeria Syndrome: Enhancing Aging Research.Aging medicine (Milton (N.S.W)) · 2025Article
- The role of different physical exercises as an anti-aging factor in different stem cells.Biogerontology · 2025Review
- Current advances and future prospects of cell reprogramming in progeroid syndromes.Frontiers in cell and developmental biology · 2025Article
- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- A Youthful Touch: Reversal of Aging Hallmarks by Cell Reprogramming.Cells, tissues, organs · 2024Review
- Embryonic stem cell-derived extracellular vesicles rejuvenate senescent cells and antagonize aging in mice.Bioactive materials · 2023Article
- Review
- Achieving single nucleotide sensitivity in direct hybridization genome imaging.Nature communications · 2022Article
- Mesenchymal stem cells derived from patients with premature aging syndromes display hallmarks of physiological aging.Life science alliance · 2022Article
- Vascular senescence in progeria: role of endothelial dysfunction.European heart journal open · 2022Article
- Article
- Review
- Alterations to Genome Organisation in Stem Cells, Their Differentiation and Associated Diseases.Results and problems in cell differentiation · 2022Article
- Telomerase therapy reverses vascular senescence and extends lifespan in progeria mice.European heart journal · 2021Article
- Review
- Opportunities and Challenges in Stem Cell Aging.Advances in experimental medicine and biology · 2021Review
- METTL3 counteracts premature aging via m6A-dependent stabilization of MIS12 mRNA.Nucleic acids research · 2020Article
- Vulnerability of progeroid smooth muscle cells to biomechanical forces is mediated by MMP13.Nature communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 7 institutions in 3 countries.
Funding
Abstract
Ideally, disease modeling using patient-derived induced pluripotent stem cells (iPSCs) enables analysis of disease initiation and progression. This requires any pathological features of the patient cells used for reprogramming to be eliminated during iPSC generation. Hutchinson-Gilford progeria syndrome (HGPS) is a segmental premature aging disorder caused by the accumulation of the truncated form of Lamin A known as Progerin within the nuclear lamina. Cellular hallmarks of HGPS include nuclear blebbing, loss of peripheral heterochromatin, defective epigenetic inheritance, altered gene expression, and senescence. To model HGPS using iPSCs, detailed genome-wide and structural analysis of the epigenetic landscape is required to assess the initiation and progression of the disease. We generated a library of iPSC lines from fibroblasts of patients with HGPS and controls, including one family trio. HGPS patient-derived iPSCs are nearly indistinguishable from controls in terms of pluripotency, nuclear membrane integrity, as well as transcriptional and epigenetic profiles, and can differentiate into affected cell lineages recapitulating disease progression, despite the nuclear aberrations, altered gene expression, and epigenetic landscape inherent to the donor fibroblasts. These analyses demonstrate the power of iPSC reprogramming to reset the epigenetic landscape to a revitalized pluripotent state in the face of widespread epigenetic defects, validating their use to model the initiation and progression of disease in affected cell lineages.
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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.