ArticleAging2014
Loss of Nfkb1 leads to early onset aging.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Pooled it
- Methylation-associated Gene Expression (MaGE): a non-invasive, in vivo measure of cellular senescence.medRxiv : the preprint server for health sciences · 2026Article
- Mice lacking NF-ĸB1 undergo premature ovarian aging.Reproductive biology and endocrinology : RB&E · 2026Article
- The Role of Dopamine Signaling and Neuroinflammation in Age-Related Cognitive Dysfunction.Brain and behavior · 2026Article
- Unraveling the intersection of aging and Parkinson's disease: a collaborative roadmap for advancing research models.NPJ Parkinson's disease · 2026Review
- Proteomic landscape of multidimensional aging phenotypes.Genome medicine · 2025Article
- Metabolic and Inflammatory Stimuli Impact Vascular Circulation and Cell Proliferation Processes in the Amygdala.Genes, brain, and behavior · 2025Article
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- A study on the association between gut microbiota, inflammation, and type 2 diabetes.Applied microbiology and biotechnology · 2024Article
- Sustained activation of NF-κB through constitutively active IKKβ leads to senescence bypass in murine dermal fibroblasts.Cell cycle (Georgetown, Tex.) · 2024Article
- Inflammaging, immunosenescence, and cardiovascular aging: insights into long COVID implications.Frontiers in cardiovascular medicine · 2024Review
- Excessive apoptosis of Rip1-deficient T cells leads to premature aging.EMBO reports · 2023Article
- Inflammation and aging: signaling pathways and intervention therapies.Signal transduction and targeted therapy · 2023Review
- Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease.Medicina (Kaunas, Lithuania) · 2022Review
- NF-κB, a culprit of both inflamm-ageing and declining immunity?Immunity & ageing : I & A · 2022Review
- p52 signaling promotes cellular senescence.Cell & bioscience · 2022Article
- Review
- Systems approaches to investigate the role of NF-κB signaling in aging.The Biochemical journal · 2022Review
- Skin manifestations of inborn errors of NF-κB.Frontiers in pediatrics · 2022Review
- The mtDNA mutation spectrum in the PolG mutator mouse reveals germline and somatic selection.BMC genomic data · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
NF-κB is a major regulator of age-dependent gene expression and the p50/NF-κB1 subunit is an integral modulator of NF-κB signaling. Here, we examined Nfkb1-/- mice to investigate the relationship between this subunit and aging. Although Nfkb1-/- mice appear similar to littermates at six months of age, by 12 months they have a higher incidence of several observable age-related phenotypes. In addition, aged Nfkb1-/- animals have increased kyphosis, decreased cortical bone, increased brain GFAP staining and a decrease in overall lifespan compared to Nfkb1+/+. In vitro, serially passaged primary Nfkb1-/- MEFs have more senescent cells than comparable Nfkb1+/+ MEFs. Also, Nfkb1-/- MEFs have greater amounts of phospho-H2AX foci and lower levels of spontaneous apoptosis than Nfkb1+/+, findings that are mirrored in the brains of Nfkb1-/- animals compared to Nfkb1+/+. Finally, in wildtype animals a substantial decrease in p50 DNA binding is seen in aged tissue compared to young. Together, these data show that loss of Nfkb1 leads to early animal aging that is associated with reduced apoptosis and increased cellular senescence. Moreover, loss of p50 DNA binding is a prominent feature of aged mice relative to young. These findings support the strong link between the NF-κB pathway and mammalian aging.
Indexed as
Identifiers
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.