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Rejuvenation Through Oxygen, More or Less
Rejuvenation Research ( IF 2.6 ) Pub Date : 2021-04-19 , DOI: 10.1089/rej.2021.0014
Shraddha M Kamat 1 , Andrew R Mendelsohn 2 , James W Larrick 2
Affiliation  

Modest modulation of oxygen intake, either by inducing mild intermittent hypoxia or hyperoxia appears to induce modest rejuvenative changes in mammals, in part, by activating key regulator hypoxia-induced factor 1a (HIF-1a). Interestingly both lower oxygen and transient higher oxygen levels induce this hypoxia regulator. Hyperbaric oxygen induces HIF-1a by the hyperoxic–hypoxic paradox that results from an overinduction of protective factors under intermittent hyperoxic conditions, leading to a state somewhat similar to that induced by hypoxia. A key difference being that SIRT1 is induced by hyperoxia, whereas it is reduced during hypoxia by the activity of HIF-1a. In a recent report, a small clinical trial employing 60 sessions of intermittent hyperbaric oxygen therapy (HBOT) studying old humans resulted in increased mean telomere length of immune cells including B cells, natural killer cells, T helper, and cytotoxic T lymphocytes. Moreover, there was a reduction in CD28null senescent T helper and cytotoxic T cells. In a parallel report, HBOT has been reported to enhance cognition in older adults, especially attention and information processing speed through increased cerebral blood flow (CBF) in brain regions where CBF tends to decline with age. The durability of these beneficial changes is yet to be determined. These preliminary results require follow-up, including more extensive characterization of changes in aging-associated biomarkers. An interesting avenue of potential work is to elucidate potential connections between hypoxia and epigenetics, especially the induction of the master pluripotent regulatory factors, which when expressed transiently have been reported to ameliorate some aging biomarkers and pathologies.

中文翻译:

通过氧气恢复活力,或多或少

通过诱导轻度间歇性缺氧或高氧对氧气摄入的适度调节似乎会诱导哺乳动物适度的恢复活力变化,部分原因是通过激活关键调节剂缺氧诱导因子 1a (HIF-1a)。有趣的是,低氧和短暂的高氧水平都会诱导这种缺氧调节剂。高压氧通过在间歇性高氧条件下过度诱导保护因子引起的高氧-低氧悖论诱导 HIF-1a,导致与缺氧诱导的状态有些相似。一个关键的区别是 SIRT1 是由高氧诱导的,而在缺氧期间它会因 HIF-1a 的活性而减少。在最近的一份报告中,一项使用 60 次间歇高压氧疗法 (HBOT) 研究老年人的小型临床试验导致免疫细胞(包括 B 细胞、自然杀伤细胞、T 辅助细胞和细胞毒性 T 淋巴细胞)的平均端粒长度增加。此外,CD28 减少衰老 T 辅助细胞和细胞毒性 T 细胞。在一份平行报告中,据报道 HBOT 可以提高老年人的认知能力,特别是通过增加脑血流量 (CBF) 来提高老年人的认知能力,而脑血流量随着年龄的增长而下降。这些有益变化的持久性还有待确定。这些初步结果需要跟进,包括对衰老相关生物标志物的变化进行更广泛的表征。一个有趣的潜在工作途径是阐明缺氧和表观遗传学之间的潜在联系,特别是主多能调节因子的诱导,据报道,当瞬时表达时,可以改善一些老化的生物标志物和病理。
更新日期:2021-04-20
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