The role of calcium homeostasis dysregulation in allergic rhinitis

The global prevalence of allergic rhinitis (AR) continues to rise, imposing a substantial burden on patient quality of life. Its pathogenesis is highly complex, encompassing immune dysregulation, compromised nasal mucosal epithelial barrier function, aberrant neuro-immune crosstalk, and disrupted epigenetic regulation. Current evidence suggests that dysregulation of calcium homeostasis may serve as a downstream effector and integrative regulatory node across multiple pathological pathways, thereby amplifying and sustaining AR-associated inflammation. This review systematically synthesizes the molecular evidence linking calcium homeostasis to the pathogenesis of AR. We summarize the regulatory roles of Ca²⁺ signaling in maintaining the nasal mucosal barrier, driving immune cell activation, and mediating neurogenic inflammation, alongside recent advances in understanding Ca²⁺ signaling-related epigenetic modifications in AR. Furthermore, integrating cross-disease evidence on transgenerational transmission in allergic diseases, we propose a novel scientific hypothesis: calcium homeostasis may modulate offspring susceptibility to AR via epigenetic mechanisms. This hypothesis offers new avenues for elucidating the transgenerational transmission of AR.