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1.
生物钟又称生物节律,是生物体内周期性波动的行为和生理现象,近年来对生物钟产生和同步的分子机制的研究日益深入.研究表明,生物钟的周期性变化与生物体的某些疾病(如失眠、癌症、抑郁症、阿尔茨海默氏病等)息息相关.所以,对生物钟与相关疾病的关系的研究有重要的意义.本文就国内外有关生物钟的生理机制及生物钟相关疾病的研究综述如下,以期为更好地研究生物钟的生理机制及防治相关疾病提供理论依据.  相似文献   

2.
目的探讨人口腔鳞癌SCC15细胞中生物钟基因PER2的表达改变对细胞增殖、凋亡以及其他生物钟基因的影响。方法用RNA干扰技术沉默人口腔鳞癌SCC15细胞中PER2基因;流式细胞术检测细胞增殖和凋亡水平;实时荧光定量PCR检测生物钟基因CLOCK、BMAL1、PER1、PER3、DEC1、DEC2、CRY1、CRY2、TIM、CKIε、RORα、NPAS2和REV-ERBαmRNA表达。结果沉默PER2后,SCC15细胞的增殖水平显著增加,凋亡显著下降(P0.05);SCC15细胞中生物钟基因PER3、BMAL1、DEC1、DEC2、CRY2、TIM、RORα和NPAS2 mRNA的表达水平显著降低,PER1和REV-ERBαmRNA的表达显著升高(P0.05)。结论在癌细胞中,生物钟基因PER2对生物钟基因网络中其他生物钟基因具有重要调控作用,PER2表达降低导致细胞增殖增加和细胞凋亡水平下降。  相似文献   

3.
在对生物钟的研究过程中,日本Nagoya大学的Ishiura等发现:蓝藻目的生物钟虽然有着同果蝇、哺乳动物及链胞霉同样的工作原理——通过蛋白质对自身基因的反馈作用而导致24小时的周期性震荡,但它的蛋白质却完全不同于其它生物。许多人认为,生物钟的进化是一个独立的过程,而并非都是由同一祖先进化而来,这一发现提供了很好的证据。为了鉴定这种蛋白质:Ishiura等通过对突变体的研究,发现了3个蓝藻目生物钟必不可少的基因:KaiA,KaiB,Kaic,它们所编码的蛋白质是蓝藻目生物钟的组成成分。这些基因通…  相似文献   

4.
生物节律是由体内的生物钟产生的。生物钟主要的分子基础是时钟基因。生物钟的主要功能是预测环境将要给予的刺激,帮助组织对即将发生的环境刺激提前作好准备。哺乳动物心血管活动具有明显的日周期节律现象,分子生物学证实心脏拥有完整的生物钟,是外周生物钟之一。生物钟节律紊乱和心血管疾病的发生和发展两者存在密切关系。  相似文献   

5.
哺乳动物的生物钟分子机制研究进展   总被引:2,自引:1,他引:1  
生物体内存在着内源性生物钟,调控着机体生命活动和生理功能。近来哺乳动物的生物钟机制的研究取得重大进展,已深入到分子水平。包括几种生物钟相关基因的分离鉴定,明确了这些基因及其蛋白质产物的功能,它们构成的自主调节的转录和翻译反馈环,是生物钟运转的分子机制。另外,哺乳动物体外培养的外周组织也存在着近日节律,这为生物节律的深入研究提供了重要线索。  相似文献   

6.
本文对生物钟基因研究的最新进展进行了综述,重点阐述了近日钟基因通过自身的转录、翻译和调控形成近日节律的过程,介绍近日钟基因在心血管系统中的重要地位。  相似文献   

7.
近年来,生物钟与骨质疏松症间的关系引起各领域研究人员的广泛兴趣。生物钟可以调节机体的节律,并维持其正常的生理功能。许多研究证实骨代谢过程同样由生物钟基因调控,一旦节律被破坏,就会导致骨量丢失,出现骨质疏松症的症状和体征。生物钟与骨质疏松症之间的密切联系也为骨质疏松症的临床防治提供了新思路。本文通过回顾过往文章,总结了生物钟影响骨代谢的途径以及骨质疏松症治疗的新路径,以期为临床上预防和治疗骨质疏松症提供参考。  相似文献   

8.
近年,时间生物学(chronobiology)的重大进展是发现调控生物周期活动的核心元件-生物钟基因:clock基因、frq基因、period基因、bmall基因timeless基因和crys基因等。生物周期是一个多层次的网络调控过程,其包括:外界信号级联、转录调控、染色质重构、转录物稳态性、蛋白质核一质穿梭、翻译调控及输出节律同步化等。在这个过程中,生物钟基因起了核心的调控作用。 在最早发现的钟基因中,clock基因和period基因(per)有以下共同特征:1)在哺乳动物中最早发现的生物钟基因,并在人的同源物上鉴定出来。2)均有哺乳动物的行为学  相似文献   

9.
生物钟紊乱与心血管疾病密切相关,无论是内源性生物钟基因改变还是外源性环境因素引起的生物钟异常均可增加心脏不良事件的发生风险,如心肌梗死、心率失常、心源性猝死等,其发生机制主要与直接影响心脏本身功能或间接影响机体整体代谢状态有关。  相似文献   

10.
生物钟可以通过影响真核生物体内基因转录、改变生物氧化还原状态等方式保证机体每天进行正常的生长代谢节律波动,人体内的生物钟还能够调控肠道免疫细胞的增殖、分化及分泌功能.生物钟紊乱时会降低机体肠道免疫系统的抗病能力进而引起局部肠道黏膜损害或部分肠道炎症的发生.由大量微生物菌群组成的肠道微环境参与机体肠道黏膜保护、能量传递及营养代谢等生理过程,微环境发生改变时也会引起肠道病理性炎症反应.昼夜节律性改变也会改变正常的肠道微生态环境,使益生菌群数量下降并激活条件致病菌,产生大量有害代谢物质引起肠道炎症反应.生物钟、肠道菌群、肠道免疫系统之间存在着一定关系,但是它们之间的联系目前并不明确.明确生物钟、肠道微环境、肠道免疫防御、炎症性肠道疾病之间关系,从而探讨肠道疾病可能的发病机制,为炎症性肠道疾病治疗途径提供新的思路治疗途径提供新的思路.  相似文献   

11.
12.
A role for CK2 in the Drosophila circadian oscillator   总被引:8,自引:0,他引:8  
The posttranslational modification of clock proteins is critical for the function of circadian oscillators. By genetic analysis of a Drosophila melanogaster circadian clock mutant known as Andante, which has abnormally long circadian periods, we show that casein kinase 2 (CK2) has a role in determining period length. Andante is a mutation of the gene encoding the beta subunit of CK2 and is predicted to perturb CK2beta subunit dimerization. It is associated with reduced beta subunit levels, indicative of a defect in alpha:beta association and production of the tetrameric alpha2:beta2 holoenzyme. Consistent with a direct action on the clock mechanism, we show that CK2beta is localized within clock neurons and that the clock proteins Period (Per) and Timeless (Tim) accumulate to abnormally high levels in the Andante mutant. Furthermore, the nuclear translocation of Per and Tim is delayed in Andante, and this defect accounts for the long-period phenotype of the mutant. These results suggest a function for CK2-dependent phosphorylation in the molecular oscillator.  相似文献   

13.
The old people often suffer from circadian rhythm disturbances, which in turn accelerate aging. Many aging-related degenerative diseases such as Alzheimer's disease, Parkinson's disease, and osteoarthritis have an inextricable connection with circadian rhythm. In light of the predominant effects of clock genes on regulating circadian rhythm, we systematically present the elaborate network of roles that clock genes play in aging in this review. First, we briefly introduce the basic background regarding clock genes. Second, we systemically summarize the roles of clock genes in aging and aging-related degenerative diseases. Third, we discuss the relationship between clock genes polymorphisms and aging. In summary, this review is intended to clarify the indispensable roles of clock genes in aging and sheds light on developing clock genes as anti-aging targets.  相似文献   

14.
A microarray analysis experiment has revealed that there are many genes, including so-called clock genes, expressing a circadian rhythm in the liver. The clock genes mentioned above are expressed not only in the suprachiasmatic nucleus (SCN) of the hypothalamus, where the master clock exists, but also in other brain regions and various peripheral tissues. In the liver, clock genes are abundantly expressed and show a clear circadian rhythm. Thus, clock genes seem to play a critical role in the molecular clockworks of both the SCN and the liver. Although oscillation of clock genes in the liver is controlled under the circadian clock mechanism in the SCN, we do not know the resetting signals on liver clock function. Over the past few years, use of the pseudorabies virus, a transsynaptic tract tracer, has allowed us to map neural connections between the SCN and peripheral tissues in several physiological systems. Communication between the SCN and peripheral tissues occurs through autonomic nervous systems involving the sympathetic and parasympathetic neurons. This review mainly describes both anatomical and physiological experiments to reveal the sympathetic control over liver clock function. Although further study is necessary to produce the precise mechanism underlying neural control of liver clock systems, evolution of this mechanism will help our understanding of liver clock functions such as drug metabolism and energy metabolism.  相似文献   

15.
The master clock in the hypothalamic suprachiasmatic nucleus (SCN) is assumed to synchronize the tissue‐specific rhythms of the peripheral clocks with the environmental day/night changes via neural, humoral and/or behavioral connections. The feeding rhythm is considered an important Zeitgeber for peripheral clocks, as daytime feeding reverses (clock) gene rhythms in the periphery, but not in the SCN. In this study, we investigated the necessity of a daily feeding rhythm for maintaining gene expression rhythms in epididymal white adipose tissue (eWAT). We showed that 7 of 9 rhythmic metabolic/adipokine genes, but not clock genes, lost their rhythmicity upon exposure to 6‐meals‐a‐day feeding. Previously, we showed comparable effects of adrenalectomy on eWAT; therefore, subsequently we investigated the effect of simultaneous disruption of these humoral and behavioral signaling pathways, by exposing adrenalectomized animals to 6‐meals‐a‐day feeding. Interestingly, under these conditions, all the clock genes and 10 of 11 rhythmic metabolic/adipokine genes lost their rhythmicity. These data indicate that adrenal hormones and feeding rhythm are indispensable for maintaining daily rhythms in metabolic/adipokine gene, but not clock gene, expression in eWAT. In contrast, at least one of these two signals should be present in order for eWAT clock gene rhythms to be maintained.  相似文献   

16.
Parkinson's disease (PD) is a common motor disorder that has become increasingly prevalent in the ageing population. Recent works have suggested that circadian rhythms disruption is a common event in PD patients. Clock genes regulate the circadian rhythm of biological processes in eukaryotic organisms, but their roles in PD remain unclear. Despite this, several lines of evidence point to the possibility that clock genes may have a significant impact on the development and progression of the disease. This review aims to consolidate recent understanding of the roles of clock genes in PD. We first summarized the findings of clock gene expression and epigenetic analyses in PD patients and animal models. We also discussed the potential contributory role of clock gene variants in the development of PD and/or its symptoms. We further reviewed the mechanisms by which clock genes affect mitochondrial dynamics as well as the rhythmic synthesis and secretion of endocrine hormones, the impairment of which may contribute to the development of PD. Finally, we discussed the limitations of the currently available studies, and suggested future potential studies to deepen our understanding of the roles of clock genes in PD pathogenesis.  相似文献   

17.
《Acta histochemica》2021,123(8):151816
The circadian clock is an endogenous timing system that ensures that various physiological processes have nearly 24 h circadian rhythms, including cell metabolism, division, apoptosis, and tumor production. In addition, results from animal models and molecular studies underscore emerging links between the cell cycle and the circadian clock. Mutations in the core genes of the circadian clock’ can disrupt the cell cycle, which in turn increases the possibility of tumors. At present, tumor chronotherapy, which relies on a circadian clock mechanism, is developing rapidly for optimizing the time of drug administration in tumor treatment to improve drug efficacy and safety. However, the relationship between the circadian clock and the cell cycle is extremely complicated. This review summarizes the possible connection between the circadian clock and the cell cycle. In addition, the review provides evidence of the influence of the circadian clock on senescence and cancer.  相似文献   

18.
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20.
In mammals, circadian oscillators exist not only in the central clock of the suprachiasmatic nucleus (SCN) but also in peripheral tissues such as the liver, heart and kidneys. Peripheral clocks are entrained to the SCN clock by both neural and humoral signals. Vitamin A might be one candidate that synchronizes peripheral clocks by activating its ligand-dependent nuclear receptors in mammals. The present study examines the effect of a Vitamin A deficiency on the circadian expression of clock genes in the mouse liver. Serum Vitamin A levels remained constant throughout the day in control mice, and were significantly reduced in Vitamin A-deficient mice. Northern blots showed that circadian expression of the clock genes mPer1, mPer2, Clock, and BMAL1, and of the clock-controlled output gene D-site binding protein (DBP), was maintained in Vitamin A-deficient mice. Our results suggest that dietary Vitamin A is not essential for generating circadian rhythms of peripheral clocks in mammals.  相似文献   

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