ReviewDisease models & mechanisms2016
Hallmarks of progeroid syndromes: lessons from mice and reprogrammed cells.
Review in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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
91 citing papers in PubMed.
- Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.Nucleus (Austin, Tex.) · 2026Article
- Article
- Review
- A manually curated gene-phenotype catalogue for progeroid syndromes and premature aging.Aging · 2026Article
- Stem cell-associated osteogenic deficiency causes craniofacial deformities with progeroid accumulation of prelamin A.JCI insight · 2026Article
- Novel genetic variants identification and immune profiling in ataxia telangiectasia patients.Journal of translational medicine · 2026Article
- POLR3A mutations cause nucleolus abnormalities and aberrant telomerase RNA metabolism in induced pluripotent stem cells from Wiedemann-Rautenstrauch premature aging syndrome patient.Biogerontology · 2025Article
- Targeting DNA damage in ageing: towards supercharging DNA repair.Nature reviews. Drug discovery · 2025Review
- Transcriptional profiling of Hutchinson-Gilford Progeria patients identifies primary target pathways of progerin.bioRxiv : the preprint server for biology · 2025Article
- Article
- Inactivation of the SLC25A1 gene during embryogenesis induces a unique senescence program controlled by p53.Cell death and differentiation · 2025Article
- Current advances and future prospects of cell reprogramming in progeroid syndromes.Frontiers in cell and developmental biology · 2025Article
- Article
- A novel role for CSA in the regulation of nuclear envelope integrity: uncovering a non-canonical function.Life science alliance · 2024Article
- Inhibition of poly(ADP-Ribosyl)ation reduced vascular smooth muscle cells loss and improves aortic disease in a mouse model of human accelerated aging syndrome.Cell death & disease · 2024Article
- Treatment of Acute and Long-COVID, Diabetes, Myocardial Infarction, and Alzheimer's Disease: The Potential Role of a Novel Nano-Compound-The Transdermal Glutathione-Cyclodextrin Complex.Antioxidants (Basel, Switzerland) · 2024Review
- miR-29 is an important driver of aging-related phenotypes.Communications biology · 2024Article
- Premature aging effects on COVID-19 pathogenesis: new insights from mouse models.Scientific reports · 2024Article
- Non-pituitary growth hormone enables colon cell senescence evasion.Aging cell · 2024Article
- Aging and cancer.Molecular cancer · 2024Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ageing is a process that inevitably affects most living organisms and involves the accumulation of macromolecular damage, genomic instability and loss of heterochromatin. Together, these alterations lead to a decline in stem cell function and to a reduced capability to regenerate tissue. In recent years, several genetic pathways and biochemical mechanisms that contribute to physiological ageing have been described, but further research is needed to better characterize this complex biological process. Because premature ageing (progeroid) syndromes, including progeria, mimic many of the characteristics of human ageing, research into these conditions has proven to be very useful not only to identify the underlying causal mechanisms and identify treatments for these pathologies, but also for the study of physiological ageing. In this Review, we summarize the main cellular and animal models used in progeria research, with an emphasis on patient-derived induced pluripotent stem cell models, and define a series of molecular and cellular hallmarks that characterize progeroid syndromes and parallel physiological ageing. Finally, we describe the therapeutic strategies being investigated for the treatment of progeroid syndromes, and their main limitations.
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