ReviewEuropean journal of histochemistry : EJH2012
Nuclear damages and oxidative stress: new perspectives for laminopathies.
Review in European journal of histochemistry : EJH, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 43 citations in OpenAlex.
- When do the pathological signs become evident? Study of human mesenchymal stem cells in MDPL syndrome.Aging · 2024Article
- The NFATc1/P2X7 receptor relationship in human intervertebral disc cells.Frontiers in cell and developmental biology · 2024Article
- Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.Frontiers in cell and developmental biology · 2023Review
- Article
- Review
- Healthful aging mediated by inhibition of oxidative stress.Ageing research reviews · 2020Review
- Oxidative Stress in Alzheimer's Disease:Oxidative medicine and cellular longevity · 2020Article
- The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage.Aging · 2019Article
- Progerin accumulation in nucleus pulposus cells impairs mitochondrial function and induces intervertebral disc degeneration and therapeutic effects of sulforaphane.Theranostics · 2019Article
- BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome.Aging · 2018Article
- Nuclear Nox4 interaction with prelamin A is associated with nuclear redox control of stem cell aging.Aging · 2018Article
- Microenvironment-Cell Nucleus Relationship in the Context of Oxidative Stress.Frontiers in cell and developmental biology · 2018Review
- Hutchinson-Gilford Progeria Syndrome: A premature aging disease caused by LMNA gene mutations.Ageing research reviews · 2017Review
- The nuclear lamina in health and disease.Nucleus (Austin, Tex.) · 2016Review
- Article
- Recent advances in understanding the role of lamins in health and disease.F1000Research · 2016Review
- Spastin and ESCRT-III coordinate mitotic spindle disassembly and nuclear envelope sealing.Nature · 2015Article
- DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.Current opinion in cell biology · 2015Review
- Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates.Nucleus (Austin, Tex.) · 2015Article
- Phenotype-Genotype Analysis of Chinese Patients with Early-Onset LMNA-Related Muscular Dystrophy.PloS one · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in genes encoding nuclear envelope proteins, particularly LMNA encoding the A-type lamins, cause a broad range of diverse diseases, referred to as laminopathies. The astonishing variety of diseased phenotypes suggests that different mechanisms could be involved in the pathogenesis of laminopathies. In this review we will focus mainly on two of these pathogenic mechanisms: the nuclear damages affecting the chromatin organization, and the oxidative stress causing un-repairable DNA damages. Alteration in the nuclear profile and in chromatin organization, which are particularly impressive in systemic laminopathies whose cells undergo premature senescence, are mainly due to accumulation of unprocessed prelamin A. The toxic effect of these molecular species, which interfere with chromatin-associated proteins, transcription factors, and signaling pathways, could be reduced by drugs which reduce their farnesylation and/or stability. In particular, inhibitors of farnesyl transferase (FTIs), have been proved to be active in rescuing the altered cellular phenotype, and statins, also in association with other drugs, have been included into pilot clinical trials. The identification of a mechanism that accounts for accumulation of un-repairable DNA damage due to reactive oxygen species (ROS) generation in laminopathic cells, similar to that found in other muscular dystrophies (MDs) caused by altered expression of extracellular matrix (ECM) components, suggests that anti-oxidant therapeutic strategies might prove beneficial to laminopathic patients.
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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.