Circadian rhythm is regulated by circadian clock, which is formed by the body response to external cyclic stimuli through the endogenous circadian clock. Circadian rhythm disturbance is closely related to the risks of a variety of diseases, and its impact on oral health cannot be ignored. Exploring the relationship and related molecular mechanism between circadian rhythm and dental hard tissues development are helpful to deeply understand the pathogenesis of developmental defects on these tissues, which could provide a theoretical basis for prevention and treatment on disorders of dental hard tissues. In order to provide guidance for the disease prevention and treatment, based on the summarization of current research progress, this paper focuses on the involvement of biorhythm in the development of tooth hard tissues as well as the disturbance of circadian rhythm on the formation of enamel and dentin, and analyzes the related regulating mechanism of circadian rhythm and genes during the development of tooth hard tissues.
Circadian Rhythm/genetics* ; Dental Enamel ; Oral Health

Circadian clock is an internal autonomous time-keeping system, including central clocks located in the suprachiasmatic nucleus (SCN) and peripheral clocks. The molecular circadian clock consists of a set of interlocking transcriptional-translational feedback loops that take the clock-controlled genes 24 h to oscillate. The core mechanism of molecular circadian clock is that CLOCK/BMAL1 dimer activates the transcription of cryptochromes (CRYs) and Periods (PERs), which act as transcriptional repressors of further CLOCK/BMAL1-mediated transcription. In addition to this basic clock, there is an additional sub-loop of REV-ERBα and RORα regulating the transcription of BMAL1. Approximately 80% protein-coding genes demonstrate significant rhythmicity. The earth rotation is responsible for the generation of the daily circadian rhythms. To coordinate metabolic balance and energy availability, almost all organisms adapt to the rhythm. Studies have shown that circadian clock integrating with metabolic homeostasis increases the efficiency of energy usage and coordinates with different organs in order to adapt to internal physiology and external environment soon. As the central organ of metabolism, the liver performs various physiological activities nearly all controlled by the circadian clock. There are multiple interactive regulation mechanisms between the circadian clock and the regulation of liver metabolism. The misalignment of metabolism with tissue circadian is identified as a high-risk factor of metabolic diseases. This article reviews the recent studies on circadian physiological regulation of liver glucose, lipid and protein metabolism and emphasizes oscillation of mitochondrial function. We also take an outlook for new methods and application of circadian clock research in the future.
CLOCK Proteins ; Circadian Clocks/genetics* ; Circadian Rhythm ; Liver ; Suprachiasmatic Nucleus

Cardiovascular Diseases ; Cardiovascular System ; Circadian Clocks/genetics* ; Circadian Rhythm ; Humans

Circadian rhythm disorder is a common society issue caused by jet lag,shift work,sleep disruption and changes in food consumption. Light is the major factor affecting the circadian rhythm system. Disruption of the circadian rhythm system can cause damage to the body,leading to some diseases. Maintaining a normal circadian system is of great importance for good health. Ideal therapeutic effect can not only alleviate symptoms of the diseases,but also recovery the disturbed circadian rhythm to normal. The paper summarizes the modeling methods of animal circadian rhythm disorder,diseases of circadian rhythm abnormality,regulation of circadian clock genes and medicine which are related to circadian rhythm to diseases of circadian rhythm disorder.
Animals ; Circadian Rhythm/genetics* ; Humans ; Jet Lag Syndrome/genetics* ; Sleep ; Sleep Disorders, Circadian Rhythm

Mammalian bone is constantly metabolized from the embryonic stage, and the maintenance of bone health depends on the dynamic balance between bone resorption and bone formation, mediated by osteoclasts and osteoblasts. It is widely recognized that circadian clock genes can regulate bone metabolism. In recent years, the regulation of bone metabolism by non-coding RNAs has become a hotspot of research. MicroRNAs can participate in bone catabolism and anabolism by targeting key factors related to bone metabolism, including circadian clock genes. However, research in this field has been conducted only in recent years and the mechanisms involved are not yet well established. Recent studies have focused on how to target circadian clock genes to treat some diseases, such as autoimmune diseases, but few have focused on the co-regulation of circadian clock genes and microRNAs in bone metabolic diseases. Therefore, in this paper we review the progress of research on the co-regulation of bone metabolism by circadian clock genes and microRNAs, aiming to provide new ideas for the prevention and treatment of bone metabolic diseases such as osteoporosis.
Animals ; Circadian Clocks/genetics* ; Circadian Rhythm/genetics* ; Mammals/genetics* ; MicroRNAs/genetics* ; Osteogenesis/genetics* ; Osteoporosis/genetics*

Circadian Rhythm/genetics* ; Gene Expression ; Humans ; Hydrocortisone ; Ischemic Stroke ; Melatonin

Studies have demonstrated that the occurrence of a variety of arrhythmias presents an obvious circadian rhythm,which may be regulated by circadian rhythm genes.Circadian cycle and light stimulation can affect circadian rhythm genes and proteins,which constitute a transcription-translation loop that can regulate the ion channels in myocardial cell membrane through nervous-humoral regulation and changes in central clock-sub-clock gene expression,thereby modulating arrhythmia.This article reviews the molecular basis,mechanism,and performance of circadian rhythm in regulating arrhythmia.
Humans ; Circadian Rhythm/genetics* ; Myocytes, Cardiac ; Arrhythmias, Cardiac

The cyanobacterial circadian clock has three relatively independent parts: the input path, the core oscillator, and the output path. The core oscillator is composed of three clock proteins: KaiA, KaiB, and KaiC. The interactions among these three proteins generate a rhythmic signal and convey the input signals to the output signals to maintain the accuracy and stability of the oscillation of downstream signals. Based on the cyanobacterial circadian clock and the structure, function, and interaction of the clock proteins of the core oscillator, combining the recent results from our laboratory, this review summarized the recent progresses of the molecular mechanism of KaiA in regulating KaiC's enzymatic activity, mediating phase reset of the oscillator, and competing with CikA for the binding site of KaiB.
Bacterial Proteins ; genetics ; metabolism ; Circadian Clocks ; genetics ; Circadian Rhythm Signaling Peptides and Proteins ; metabolism ; Cyanobacteria ; genetics ; Enzyme Activation ; genetics

Smith-Magenis syndrome (SMS) (OMIM #182290) is a rare genetic disorder with a prevalence of 1 in 25 000 live births. Approximately 90% of SMS patients have harbored a 3.7 Mb interstitial 17p11.2 deletion involving the RAI1 gene, while 10% of cases have carried pathogenic variants of the RAI1 gene. SMS is characterized by sleep disturbance, intellectual impairment, developmental delay, craniofacial and cardiovascular anomalies, obesity, self injury, aggressive and autistic-like behaviors. Most SMS patients have sleep disorders such as short total sleep time, frequent night waking, short sleep onset, and early morning waking. The sleep disturbance may aggravate with age and persist throughout life. Three mechanisms have been delineated. The first concern was the abnormal secretion of melatonin, with high levels during daytime and low levels at night. Evaluation of the integrity of the intrinsically photosensitive retinal ganglion cell (ipRGC)/melanopsin system has found that SMS patients showed dysfunction in the sustained component of the pupillary light responses to blue light. Synchronization of daily melatonin profile and its photoinhibition are dependent on the activation of melanopsin. Dysfunction of the retina-melanin system may be one of the causes of melatonin spectrum disorders. Secondly, dysregulation of circadian rhythm gene expression has also been noted in mice and SMS patients. Finally, there may be association between sleep deprivation symptoms and DNA methylation patterns, which has provided new insights for SMS-associated sleep disorders and symptoms alike. Treatment for SMS-related sleep disorders is administered primarily through medications like melatonin tablets, which can alleviate insomnia-related sleep difficulties, in particular externalizing behavior in children. Researchers are also actively exploring other treatments for SMS currently.
Animals ; Circadian Rhythm ; Humans ; Melatonin ; Mice ; Sleep ; Sleep Wake Disorders/genetics* ; Smith-Magenis Syndrome/genetics*

OBJECTIVETo investigate the molecular biological mechanism of chronoexercise regulating circadian.

METHODSExpressions of mPer1 and mPer2 in the diencephalon of golden hamster were determined 2 hours after acute exhaustive exercise (circadian time 6) by quantitative RT-PCR.

RESULTSChronoexercise at CT6 significantly decreased expressions of mPer1 and mPer2 in the diencephalon of golden hamster.

CONCLUSIONInhibitory effect of chronoexercise on Per1 and Per2 mRNA levels in the diencephalon of golden hamster at CT6 may be achieved transcription-translation-based autoregulatory negative feedback loop.

Animals ; Circadian Rhythm ; physiology ; Cricetinae ; Gene Expression ; Period Circadian Proteins ; genetics ; metabolism ; Physical Conditioning, Animal ; RNA, Messenger ; genetics ; Reverse Transcriptase Polymerase Chain Reaction