ArticleNature aging2023
Nuclear envelope disruption triggers hallmarks of aging in lung alveolar macrophages.
Article in Nature aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Integration of nuclear mechanosensing with integrin-extracellular matrix adhesions.Nucleus (Austin, Tex.) · 2026Review
- Nuclear envelope rupture and resealing: mechanisms, consequences, and disease implications.Biochemical Society transactions · 2026Review
- The Underexplored Mechanobiology of Lamin A Biogenesis and Homeostasis.Biology of the cell · 2026Review
- Single-cell immune atlas of mouse testes unveils metabolic reprogramming of FOLR2 + macrophages in orchestrating testicular immunity during aging.GeroScience · 2026Article
- Age-associated decline of Lamtor5 drives immunosenescence and systemic aging via cGAS-mediated paracrine inflammation.Cell death and differentiation · 2026Article
- Epigenetic de-repression of basal cell metaplasia in aging AT2 cells is a risk factor for idiopathic pulmonary fibrosis (IPF).bioRxiv : the preprint server for biology · 2026Article
- Lipid droplets are rigid and physically suppress phagocytosis, unless cell compression or stretching activates actomyosin.Molecular biology of the cell · 2026Article
- A Comprehensive Review of Nuclear Mechanics: Advances, Disease Relevance, Methodologies, and AI Applications.Cell biochemistry and biophysics · 2026Review
- Dynamins maintain nuclear envelope homeostasis and genome stability.Nature communications · 2026Article
- ACBP/DBI Neutralization Stimulates Anticancer Immune Responses by Upregulating Lamin A in T Cells.ImmunoTargets and therapy · 2026Article
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- Article
- Immunosenescence and cancer: molecular hallmarks, tumor microenvironment remodeling, and age-specific immunotherapy challenges.Journal of hematology & oncology · 2025Review
- Cancer-associated SPOP mutations enlarge nuclear size and facilitate nuclear envelope rupture upon farnesyltransferase inhibitor treatment.The Journal of clinical investigation · 2025Article
- A Single-Cell Transcriptome Atlas Characterizes the Immune Landscape of Human Testes During Aging.Aging cell · 2025Article
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- Reevaluating Anti-Inflammatory Therapy: Targeting Senescence to Balance Anti-Cancer Efficacy and Vascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Lysosomes in the immunometabolic reprogramming of immune cells in atherosclerosis.Nature reviews. Cardiology · 2025Review
- Senescent Macrophages and the Lung Cancer Microenvironment: A New Perspective on Tumor Immune Evasion.Aging and disease · 2024Review
- Role of lamin A/C on dendritic cell function in antiviral immunity.Cellular and molecular life sciences : CMLS · 2024Article
Corrections and comments
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Authors and funding
27 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is characterized by gradual immune dysfunction and increased disease risk. Genomic instability is considered central to the aging process, but the underlying mechanisms of DNA damage are insufficiently defined. Cells in confined environments experience forces applied to their nucleus, leading to transient nuclear envelope rupture (NER) and DNA damage. Here, we show that Lamin A/C protects lung alveolar macrophages (AMs) from NER and hallmarks of aging. AMs move within constricted spaces in the lung. Immune-specific ablation of lamin A/C results in selective depletion of AMs and heightened susceptibility to influenza virus-induced pathogenesis and lung cancer growth. Lamin A/C-deficient AMs that persist display constitutive NER marks, DNA damage and p53-dependent senescence. AMs from aged wild-type and from lamin A/C-deficient mice share a lysosomal signature comprising CD63. CD63 is required to limit damaged DNA in macrophages. We propose that NER-induced genomic instability represents a mechanism of aging in AMs.
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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.