2014
DOI: 10.18632/aging.100702
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Abstract: NF-(B is a major regulator of age-dependent gene expression and the p50/NF-(B1 subunit is an integral modulator of NF-(B 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 dec… Show more

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Cited by 72 publications
(65 citation statements)
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References 48 publications
(69 reference statements)
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“…Chronic inflammation is a hallmark of aging, and is found also in patients with progeria [78,79]. Furthermore, it was recently shown that chronic inflammation in mice, caused by ablation of NF-kB subunits p50 and p105 (leading to NF-kB activation), can lead to telomere dysfunction and accelerated aging, mediated by an increased rate of cellular senescence [80]. Other mouse models of progeria are also associated with NF-kB activation: in Zmpste24 -/-and Lamin A/C (LMNA) mutant mice, a farnesylated form of pre-Lamin A accumulates at the nuclear envelope, causing nuclear abnormalities and cellular senescence [81][82][83].…”
Section: Feature Reviewmentioning
confidence: 99%
“…Chronic inflammation is a hallmark of aging, and is found also in patients with progeria [78,79]. Furthermore, it was recently shown that chronic inflammation in mice, caused by ablation of NF-kB subunits p50 and p105 (leading to NF-kB activation), can lead to telomere dysfunction and accelerated aging, mediated by an increased rate of cellular senescence [80]. Other mouse models of progeria are also associated with NF-kB activation: in Zmpste24 -/-and Lamin A/C (LMNA) mutant mice, a farnesylated form of pre-Lamin A accumulates at the nuclear envelope, causing nuclear abnormalities and cellular senescence [81][82][83].…”
Section: Feature Reviewmentioning
confidence: 99%
“…Genetic deletion of p50/p105 can lead to premature aging [45], age-related neuronal degeneration [46], accelerated noise-induced hearing loss [47], and the development of spontaneous optic neuropathy [48,49]. Importantly, Bernal and coworkers [45] have shown that aged Nfkb1-ko mice display a decrease in spontaneous apoptosis in the brain, increase in cellular DNA damage and increased astrogliosis. Thus, we cannot exclude the possibility that despite the higher level of neuronal preservation in the hippocampus, Nfkb1-ko mice in our study displayed higher level of cellular senescence not detected by our immunohistochemical methods.…”
Section: Discussionmentioning
confidence: 99%
“…Новейшие данные показывают, что нарушения регуляции активности NF-kb ассоциированы с укорочением длительности жизни [33]. Нарушения активности сигнального пути Wnt, который также содержит магний-зависимые белки, ассоциированы с развитием нейродегенеративных заболеваний [34].…”
Section: заключениеunclassified