Maiese Kenneth
Cellular and Molecular Signaling, Newark, NY. United States.
Curr Neurovasc Res. 2017;14(3):299-304. doi: 10.2174/1567202614666170718092010.
The mammalian circadian clock and its associated clock genes are increasingly been recognized as critical components for a number of physiological and disease processes that extend beyond hormone release, thermal regulation, and sleep-wake cycles. New evidence suggests that clinical behavior disruptions that involve prolonged shift work and even space travel may negatively impact circadian rhythm and lead to multi-system disease.
In light of the significant role circadian rhythm can hold over the body's normal physiology as well as disease processes, we examined and discussed the impact circadian rhythm and clock genes hold over lifespan, neurodegenerative disorders, and tumorigenesis.
In experimental models, lifespan is significantly reduced with the introduction of arrhythmic mutants and leads to an increase in oxidative stress exposure. Interestingly, patients with Alzheimer's disease and Parkinson's disease may suffer disease onset or progression as a result of alterations in the DNA methylation of clock genes as well as prolonged pharmacological treatment for these disorders that may lead to impairment of circadian rhythm function. Tumorigenesis also can occur with the loss of a maintained circadian rhythm and lead to an increased risk for nasopharyngeal carcinoma, breast cancer, and metastatic colorectal cancer. Interestingly, the circadian clock system relies upon the regulation of the critical pathways of autophagy, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), and silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) as well as proliferative mechanisms that involve the wingless pathway of Wnt/β-catenin pathway to foster cell survival during injury and block tumor cell growth.
Future targeting of the pathways of autophagy, mTOR, SIRT1, and Wnt that control mammalian circadian rhythm may hold the key for the development of novel and effective therapies against aging- related disorders, neurodegenerative disease, and tumorigenesis.
哺乳动物生物钟及其相关的时钟基因越来越被认为是许多生理和疾病过程的关键组成部分,这些过程不仅包括激素释放、体温调节和睡眠 - 觉醒周期。新证据表明,涉及长期轮班工作甚至太空旅行的临床行为干扰可能会对昼夜节律产生负面影响,并导致多系统疾病。
鉴于昼夜节律对身体正常生理以及疾病过程具有重要作用,我们研究并讨论了昼夜节律和时钟基因对寿命、神经退行性疾病和肿瘤发生的影响。
在实验模型中,引入无节律突变体后寿命显著缩短,并导致氧化应激暴露增加。有趣的是,阿尔茨海默病和帕金森病患者可能由于时钟基因的DNA甲基化改变以及针对这些疾病的长期药物治疗导致昼夜节律功能受损而发病或病情进展。昼夜节律紊乱也可导致肿瘤发生,并增加鼻咽癌、乳腺癌和转移性结直肠癌的风险。有趣的是,昼夜节律系统依赖于自噬、雷帕霉素靶蛋白(mTOR)、AMP激活蛋白激酶(AMPK)和沉默信息调节因子2同源物1(酿酒酵母)(SIRT1)等关键途径的调节,以及涉及Wnt/β - 连环蛋白途径中无翅通路的增殖机制,以促进损伤时的细胞存活并阻止肿瘤细胞生长。
未来针对控制哺乳动物昼夜节律的自噬、mTOR、SIRT1和Wnt途径进行靶向治疗,可能是开发针对衰老相关疾病、神经退行性疾病和肿瘤发生的新型有效疗法的关键。