ArticleNucleus (Austin, Tex.)
Oxydative stress alters nuclear shape through lamins dysregulation: a route to senescence.
Article in Nucleus (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Detection of nuclear STING in cultured human cells and in the normal and cancer tissues.iScience · 2026Article
- Article
- Clinical and metabolic consequences of a historic pathogenic lamin A/C founder variant.Scientific reports · 2025Article
- Review
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- Drosophila female germline stem cells undergo mitosis without nuclear breakdown.Current biology : CB · 2021Article
- Review
- Metabolic choreography of gene expression: nutrient transactions with the epigenome.Journal of biosciences · 2020Review
- On the epigenetic role of guanosine oxidation.Redox biology · 2020Review
- Synaptic deficits in iPSC-derived cortical interneurons in schizophrenia are mediated by NLGN2 and rescued by N-acetylcysteine.Translational psychiatry · 2019Article
- The three-dimensional organization of the genome in cellular senescence and age-associated diseases.Seminars in cell & developmental biology · 2019Review
- Lamin B is a target for selective nuclear PQC by BAG3: implication for nuclear envelopathies.Cell death & disease · 2019Article
- Nuclear Nox4 interaction with prelamin A is associated with nuclear redox control of stem cell aging.Aging · 2018Article
- Nuclear lamina dysfunction triggers a germline stem cell checkpoint.Nature communications · 2018Article
- Independent Mechanisms Lead to Genomic Instability in Hodgkin Lymphoma: Microsatellite or Chromosomal InstabilityCancers · 2018Article
- Glutathione Peroxidase 3 Delivered by hiPSC-MSCs Ameliorated Hepatic IR Injury via Inhibition of Hepatic Senescence.Theranostics · 2018Article
- Microenvironment-Cell Nucleus Relationship in the Context of Oxidative Stress.Frontiers in cell and developmental biology · 2018Review
- Phytochemical-induced nucleolar stress results in the inhibition of breast cancer cell proliferation.Redox biology · 2017Article
- Article
- Altered DNA methylation associated with an abnormal liver phenotype in a cattle model with a high incidence of perinatal pathologies.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progeroid phenotypes are mainly encountered in 2 types of syndromes: in laminopathies, which are characterized by nuclear shape abnormalities due to lamin A alteration, and in DNA damage response defect syndromes. Because lamin A dysregulation leads to DNA damages, it has been proposed that senescence occurs in both types of syndromes through the accumulation of damages. We recently showed that elevated oxidative stress is responsible for lamin B1 accumulation, nuclear shape alteration and senescence in the DDR syndrome, ataxia telangiectasia (A-T). Interestingly, overexpression of lamin B1 in wild type cells is sufficient to induce senescence without the induction of DNA damages. Here, we will discuss the importance of controlling the lamins level in order for maintenance nuclear architecture and we will comment the relationships of lamins with other senescence mechanisms. Finally, we will describe emerging data reporting redox control by lamins, leading us to propose a general mechanism by which reactive oxygen species can induce senescence through lamin dysregulation and NSA.
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