The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index.
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
In the citing paper
“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]
In the citing paper
“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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Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Shared Principles in NF-κB Signaling
Hayden, M. S., & Ghosh, S. (2008) · Cell · doi:10.1016/j.cell.2008.01.020 · Cited by 4,954
Schreiber, E. H., Matthias, P., Müller, M. M., & Schaffner, W. (1989) · Nucleic Acids Research · doi:10.1093/nar/17.15.6419 · Cited by 4,179
Prostaglandins and Inflammation
Ricciotti, E., & FitzGerald, G. A. (2011) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.110.207449 · Cited by 4,035
NF-κB regulation in the immune system
Li, Q., & Verma, I. M. (2002) · Nature Reviews Immunology · doi:10.1038/nri910 · Cited by 4,007
NF-κB: a key role in inflammatory diseases
Tak, P. P., & Firestein, G. S. (2001) · Journal of Clinical Investigation · doi:10.1172/jci11830 · Cited by 3,918
Hayden, M. S., & Ghosh, S. (2004) · Genes & Development · doi:10.1101/gad.1228704 · Cited by 3,842
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670 · cited 2×
“Since a proper clearance of senescent cells by the immune system seems to be crucial for homeostasis maintenance in aging and cancer (Baker et al. 2011; Kang et al. 2011), both NF-kB hyperactivation and the subsequent age-related immunological decline could be compromising an appropriate response against age-accumulat…”
BackgroundIntegrating cell-signalling pathways with NF-κB and IKK function
Perkins, N. D. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2083 · Cited by 2,350
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Items 101–101 of 101
González‐Dominguez, A., Montañez, R., Castejón‐Vega, B., Nuñez‐Vasco, J., Lendines‐Cordero, D., Wang, C., Mbalaviele, G., Navarro‐Pando, J. M., Alcocer‐Gómez, E., & Cordero, M. D. (2021) · EMBO Molecular Medicine · doi:10.15252/emmm.202114012 · Cited by 32
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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