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Nuclear lamina defects cause ATM-dependent NF-κB activation and link accelerated aging to a systemic inflammatory response
Open accessAbstract
Alterations in the architecture and dynamics of the nuclear lamina have a causal role in normal and accelerated aging through both cell-autonomous and systemic mechanisms. However, the precise nature of the molecular cues involved in this process remains incompletely defined. Here we report that the accumulation of prelamin A isoforms at the nuclear lamina triggers an ATM- and NEMO-dependent signaling pathway that leads to NF-κB activation and secretion of high levels of proinflammatory cytokines in two different mouse models of accelerated aging (Zmpste24−/− and Lmna G609G/G609G mice). Causal involvement of NF-κB in accelerated aging was demonstrated by the fact that both genetic and pharmacological inhibition of NF-κB signaling prevents age-associated features in these animal models, significantly extending their longevity. Our findings provide in vivo proof of principle for the feasibility of pharmacological modulation of the NF-κB pathway to slow down the progression of physiological and pathological aging.
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“Restoration of the somatotrophic axis through hormonal treatments or inhibition of NF-κB signaling also extends lifespan in these progeroid mice (Marino et al., 2010; Osorio et al., 2012).”
From The Hallmarks of Aging (2013) · cites this paper as Osorio et al., 2012
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“genetic and pharmacological inhibition of NF-κB signaling prevents age-associated features in different mouse models of accelerated aging”
From The Hallmarks of Aging (2013) · cites this paper as Osorio et al., 2012
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“In mouse models of accelerated ageing, inflammation is exacerbated by the overactivation of NF-κB, thereby blocking this pathway and consequently conferring longevity.475”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [475]
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“Inhibition of NF-κB signalling (the main transcription factor regulating the SASP) both genetically and pharmacologically, has been shown to prevent age-related deterioration in progeroid mouse models (Osorio et al., 2012).”
From Stress, cell senescence and organismal ageing (2018) · cites this paper as Osorio et al., 2012
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“In addition, based on our study and those of others, ATM inhibition could also be efficacious in the setting of other diseases involving oxidative stress and proinflammatory cytokines including inflammation, angiogenesis and aging (Osorio et al., 2012; Okuno et al., 2012).”
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Metadata
- Authors
- Osorio, F. G., Bárcena, C., Soria-Valles, C., Ramsay, A. J., de Carlos, F., Cobo, J., Fueyo, A., Freije, J. M. P., & López-Otín, C.
- Affiliations
- Universidad de Oviedo (ES)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-09-26
- Volume
- 26
- Issue
- 20
- Pages
- 2311-2324
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3475803
- OpenAlex
- W2101185010
- Cited by
- 276
- References
- 76
- Citations by year
- 2026: 7 · 2025: 19 · 2024: 18 · 2023: 11 · 2022: 21 · 2021: 21 · 2020: 17 · 2019: 26 · 2018: 33 · 2017: 18 · 2016: 27 · 2015: 22 · 2014: 19 · 2013: 16 · 2012: 1
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Consultation of the Doctoral Thesis Database (TESEO) (Ministerio de Educación, Cultura y Deporte) (submittedVersion, cc-by-nc-nd)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-nd)
- Funders
- European Commission
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- nuclear lamina, accelerated aging, NF-κB activation, ATM signaling, NEMO, prelamin A, lamin A/C, inflammatory cytokines, systemic inflammation, ZMPSTE24, laminopathies, longevity
- MeSH terms
- Aging, Animals, Anti-Inflammatory Agents, Non-Steroidal, Cell Line, Cells, Cultured, DNA-Binding Proteins, Humans, Inflammation, Longevity, Membrane Proteins, Metalloendopeptidases, Nuclear Proteins, Protein Precursors, Sodium Salicylate, Signal Transduction, Transcriptional Activation, NF-kappa B, Cellular Senescence, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Tumor Suppressor Proteins, Nuclear Lamina, Lamin Type A, Intracellular Signaling Peptides and Proteins, Mice, Transcription Factor RelA, Ataxia Telangiectasia Mutated Proteins
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