ArticleAging cell2018
Altered modulation of lamin A/C-HDAC2 interaction and p21 expression during oxidative stress response in HGPS.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure.Nature communications · 2020Pooled it
- Nucleoplasmic Lamin A/C controls replication fork restart upon stress by modulating local H3K9me3 and ADP-ribosylation levels.Nature communications · 2025Article
- Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson-Gilford Progeria Syndrome.Diseases (Basel, Switzerland) · 2025Article
- Cardiac phenotypes in LMNA mutations.Current opinion in cardiology · 2025Review
- Review
- Tubular Lamin- and Emerin-Lined Nuclear Envelope Invaginations Isolate Chromatin Domains for Gene Expression Regulation.Sub-cellular biochemistry · 2025Review
- Disorganized chromatin hierarchy and stem cell aging in a male patient of atypical laminopathy-based progeria mandibuloacral dysplasia type A.Nature communications · 2024Article
- LAP2alpha facilitates myogenic gene expression by preventing nucleoplasmic lamin A/C from spreading to active chromatin regions.Nucleic acids research · 2024Article
- Article
- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- Microbiota derived D-malate inhibits skeletal muscle growth and angiogenesis during aging via acetylation of Cyclin A.EMBO reports · 2024Article
- Dexamethasone induces p21FEBS open bio · 2023Article
- Article
- Global crotonylome reveals hypoxia-mediated lamin A crotonylation regulated by HDAC6 in liver cancer.Cell death & disease · 2022Article
- Article
- The role of prelamin A post-translational maturation in stress response and 53BP1 recruitment.Frontiers in cell and developmental biology · 2022Article
- Nuclear envelope, chromatin organizers, histones, and DNA: The many achilles heels exploited across cancers.Frontiers in cell and developmental biology · 2022Review
- ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.Frontiers in cell and developmental biology · 2022Article
- Nuclear mechanosensing drives chromatin remodelling in persistently activated fibroblasts.Nature biomedical engineering · 2021Article
- Lamin post-translational modifications: emerging toggles of nuclear organization and function.Trends in biochemical sciences · 2021Review
Corrections and comments
- Erratum issuedCorrigendum.2018
Authors and funding
14 authors at 8 institutions in 3 countries.
Funding
Abstract
Defects in stress response are main determinants of cellular senescence and organism aging. In fibroblasts from patients affected by Hutchinson-Gilford progeria, a severe LMNA-linked syndrome associated with bone resorption, cardiovascular disorders, and premature aging, we found altered modulation of CDKN1A, encoding p21, upon oxidative stress induction, and accumulation of senescence markers during stress recovery. In this context, we unraveled a dynamic interaction of lamin A/C with HDAC2, an histone deacetylase that regulates CDKN1A expression. In control skin fibroblasts, lamin A/C is part of a protein complex including HDAC2 and its histone substrates; protein interaction is reduced at the onset of DNA damage response and recovered after completion of DNA repair. This interplay parallels modulation of p21 expression and global histone acetylation, and it is disrupted by LMNAmutations leading to progeroid phenotypes. In fact, HGPS cells show impaired lamin A/C-HDAC2 interplay and accumulation of p21 upon stress recovery. Collectively, these results link altered physical interaction between lamin A/C and HDAC2 to cellular and organism aging. The lamin A/C-HDAC2 complex may be a novel therapeutic target to slow down progression of progeria symptoms.
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What OpenQuestion holds
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.