ReviewBiochemical Society transactions2020
Towards delineating the chain of events that cause premature senescence in the accelerated aging syndrome Hutchinson-Gilford progeria (HGPS).
Review in Biochemical Society transactions, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- A manually curated gene-phenotype catalogue for progeroid syndromes and premature aging.Aging · 2026Article
- Unraveling the mysteries of Hutchinson-Gilford progeria syndrome: a comprehensive review of LMNA gene mutations.Biogerontology · 2025Review
- Progerin Can Induce DNA Damage in the Absence of Global Changes in Replication or Cell Proliferation.bioRxiv : the preprint server for biology · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Genetic and pharmacological modulation of lamin A farnesylation determines its function and turnover.Aging cell · 2024Article
- Progerin can induce DNA damage in the absence of global changes in replication or cell proliferation.PloS one · 2024Article
- Prelamin A and ZMPSTE24 in premature and physiological aging.Nucleus (Austin, Tex.) · 2023Review
- The E262K mutation in Lamin A links nuclear proteostasis imbalance to laminopathy-associated premature aging.Aging cell · 2022Article
- Lamin A to Z in normal aging.Aging · 2022Article
- MG132 Induces Progerin Clearance and Improves Disease Phenotypes in HGPS-like Patients' Cells.Cells · 2022Article
- Genetic basis of cardiovascular aging is at the core of human longevity.The journal of cardiovascular aging · 2022Article
- More Than Skin Deep - the Effects of Ultraviolet Radiation on Cathepsin K and Progerin Expression in Cultured Dermal Fibroblasts.Clinical, cosmetic and investigational dermatology · 2021Article
- The impact of alterations in lamin A on genome integrity.Mutation research. Reviews in mutation researchReview
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
The metazoan nucleus is equipped with a meshwork of intermediate filament proteins called the A- and B-type lamins. Lamins lie beneath the inner nuclear membrane and serve as a nexus to maintain the architectural integrity of the nucleus, chromatin organization, DNA repair and replication and to regulate nucleocytoplasmic transport. Perturbations or mutations in various components of the nuclear lamina result in a large spectrum of human diseases collectively called laminopathies. One of the most well-characterized laminopathies is Hutchinson-Gilford progeria (HGPS), a rare segmental premature aging syndrome that resembles many features of normal human aging. HGPS patients exhibit alopecia, skin abnormalities, osteoporosis and succumb to cardiovascular complications in their teens. HGPS is caused by a mutation in LMNA, resulting in a mutated form of lamin A, termed progerin. Progerin expression results in a myriad of cellular phenotypes including abnormal nuclear morphology, loss of peripheral heterochromatin, transcriptional changes, DNA replication defects, DNA damage and premature cellular senescence. A key challenge is to elucidate how these different phenotypes are causally and mechanistically linked. In this mini-review, we highlight some key findings and present a model on how progerin-induced phenotypes may be temporally and mechanistically linked.
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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.