Abstract: Atopic dermatitis (AD) is a chronic and recurrent inflammatory skin disease characterized by circadian fluctuations in clinical symptoms, especially pruritus, and physiological parameters such as transepidermal water loss. Circadian disruption may contribute to the onset and progression of AD by disturbing skin barrier homeostasis, immune inflammatory responses, and neuroendocrine regulation. This review summarizes the potential mechanisms underlying circadian regulation in AD. Abnormal oscillations of the core clock genes CLOCK/BMAL1 may impair the rhythmic expression of barrier-related molecules, including aquaporin-3 (AQP3) and filaggrin, thereby weakening nocturnal skin barrier defense. The circadian clock interacts bidirectionally with type 2 inflammation; inflammatory cytokines may interfere with clock gene expression through molecules such as EGR1, whereas abnormalities of clock-related genes, including NR1D1 in dendritic cells, may promote Th2 immune polarization. Disordered melatonin signaling, disrupted cortisol rhythms, and metabolic remodeling may collectively reduce the nocturnal itch threshold and increase oxidative stress. This paper reviews the mechanisms by which circadian rhythms regulate AD, and analyzes chronotherapeutic strategies including timed medication, melatonin intervention, light exposure and sleep management.

Key words: atopic dermatitis, circadian rhythm, clock genes, skin barrier, chronotherapy