Research Progress on the Effect of Circadian Rhythm Disruption on the Pathogenesis of Chronic Atrophic Gastritis

Abstract

The circadian rhythm, as a crucial endogenous regulatory mechanism for organisms to adapt to periodic changes in the external environment, is closely related to the occurrence and development of various digestive system diseases when disrupted. Recent studies have found that patients with chronic atrophic gastritis (CAG) commonly exhibit manifestations of circadian rhythm disruption such as sleep disorders and irregular meal times, suggesting that abnormalities in clock genes may participate in the pathological process of CAG by regulating the rhythm of gastric acid secretion, gastric mucosal barrier repair, and inflammatory response pathways. Aberrant expression of core clock genes BMAL1 and CLOCK can disrupt the balance between gastric epithelial cell proliferation and apoptosis, while disrupted melatonin secretion may exacerbate oxidative stress damage to the gastric mucosa. Animal experiments have confirmed that long-term alterations in the light-dark cycle or knockout of clock genes can induce gastric mucosal atrophy and intestinal metaplasia, with the activation of signaling pathways such as NF-κB and MAPK playing a key role in this process. Clinical studies further reveal a significantly higher incidence of CAG among shift workers, showing a dose-response relationship with abnormalities in rhythm-related hormone levels. Current evidence supporting the application of rhythm interventions, such as timed feeding and light therapy, in the prevention and treatment of CAG requires further high-quality validation. Future research needs to deeply explore mechanisms such as the epigenetic regulation of clock genes and the microbiota-circadian axis interaction to provide a theoretical basis for developing chronotherapy-based strategies for CAG prevention and treatment.