ARNTL (Aryl Hydrocarbon Receptor Nuclear Translocator Like)

In contrast, restoring complex I function by expressing yeast NDI1 in adipocytes protects against diet-induced and circadian-induced metabolic dysfunction independently of weight gain. These findings reveal that adipocyte circadian disruption impairs metabolic health through mitochondrial complex I dysfunction, establishing clock control of complex I as a key regulator of metabolic homeostasis.

Overexpression of LINC02159 or ARNTL2 partially reversed the pro-ferroptotic effects of METTL7B knockdown on NSCLC cells. In conclusion, METTL7B inhibits ferroptosis in NSCLC cells via the LINC02159/KAT2A/ARNTL2 axis in an m6A-dependent manner.

This study revealed a novel mechanism in which BMAL1 downregulation under aging and HFD conditions promotes NASH progression by binding to HIF-1α and modulating the glycolysis-NLRP3 inflammasome axis.

We emphasize the associations between circadian disruption and CRC-including diagnostic markers, prognostic assessment, and chemosensitivity-and provide an in-depth discussion of chronotherapeutic strategies and their translational potential. Finally, we identify unaddressed scientific questions and propose future research directions to facilitate the development of novel targeted therapies for CRC.

The expression levels of ARNTL2 and miR-204-5p in NSCLC are closely associated with patient age, tumor differentiation, and lymph node metastasis, and they have high predictive value for NSCLC-related mortality.

FlyDEGdb stores information on changes in the expression of the dysf gene and its homologues: (a) the Clk, cyc, and per genes in Drosophila, and (b) the NPAS4, CLOCK, BMAL1, PER1, and PER2 genes in humans. These data are supplemented with information on the biological processes in which these genes are involved: oocyte maturation (oogenesis), regulation of stress response and circadian rhythm, carcinogenesis, aging, etc. Therefore, FlyDEGdb, containing information on the widely used model organism, Drosophila, can be helpful for researchers working in the molecular biology and genetics of humans and animals, physiology, translational medicine, pharmacology, dietetics, agricultural chemistry, radiobiology, toxicology, and bioinformatics.

Based on these findings, the theory of "Taiyin disease resolution period" provides guidance for chronotherapeutic intervention in CAG management. Through innovative integration of modern chronobiology and traditional temporal medicine principles, the study illuminates the central role of the circadian clock gene in the CAG "inflammation to cancer" transformation and emphasizes the potential of the circadian clock and chronotherapy in reversing the "inflammation to cancer" transformation, offering both mechanistic insights and clinically actionable strategies for CAG treatment via chronobiology.

Consistent with functional tuning, treatment of myotubes with serum collected from Bmal1hep-/- mice during the dark phase lowers mitochondrial ATP production compared with serum from wild-type mice. Overall, our results reveal communication between the liver clock and skeletal muscle, uncovering a bidirectional endocrine communication pathway that may contribute to the metabolic phenotypes of circadian disruption.

Targeting the circadian clock or fatty acid desaturation augmented cuproptosis antitumor effects. Crosstalk between the core circadian clock and copper sustains GSCs, reshaping fatty acid metabolism and promoting drug resistance, which may inform development of combination therapies for GBM.

Recent findings demonstrate that time-of-day-dependent administration of vaccines and immunotherapies, including checkpoint inhibitors, can significantly influence clinical efficacy and immune outcomes. Understanding the temporal orchestration of adaptive immunity thus holds translational potential for optimizing therapeutic strategies, including chronotherapy and vaccination scheduling.

In addition, clock gene expression profiles emerge as independent prognostic biomarkers for CRC. Future research needs to integrate multiple omics datasets, and artificial intelligence models can analyze the circadian regulation network in CRC, providing new ideas for the precise prevention and treatment of CRC.

A mechanistic pharmacokinetic-pharmacodynamic model incorporating the clock network recapitulated experimental observations and enabled prediction of treatment timing. Our findings highlight the importance of timing in GBM therapy and propose combining circadian profiling with mathematical modeling to personalize GBM chronotherapy.