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Ion channel dysfunction in acute pancreatitis: mechanisms, heterogeneity, and therapeutic prospects
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DOI：10.1016/j.trsl.2026.06.016.png)
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Abstract
En 中文
Acute pancreatitis (AP) is a life-threatening gastrointestinal disorder with rising global incidence and persistently high mortality, currently lacking disease-modifying therapies and resulting in substantial unmet clinical needs. Ion channel and transporter dysfunction is proposed as a convergent mechanistic link within a subset of etiologies, driving conserved pathological cascades such as intracellular calcium overload, mitochondrial dysfunction, secretory insufficiency, and systemic inflammation. Building upon prior studies of individual ion channels, this review systematically integrates current evidence within a network-centric framework to provide new insights into ion-mediated AP pathogenesis. Recognizing the etiological heterogeneity and translational barriers, this review emphasizes the convergent pathogenic role of ionic dysregulation in specific pathophysiological contexts and underscores the clinical potential of precision-targeted ion-modulating therapies for AP prevention and treatment.
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