TMEM16A Ca2+-activated Cl- channel inhibition ameliorates acute pancreatitis via the IP3R/Ca2+/NFκB/IL-6 signaling pathway

This study identifies a novel mechanism underlying the pathogenesis of AP by which IL-6 promotes TMEM16A expression via IL-6R/STAT3 signaling activation, and TMEM16A overexpression increases IL-6 secretion via IP3R/Ca2+/NFκB signaling activation in pancreatic acinar cells. TMEM16A inhibition may be a new potential strategy for treating AP.Graphical abstractA positive activation loop between TMEM16A and the IP3R/ Ca2+/NFκB/IL-6 pathway is important for Ca2+ elevation, NFκB activation and IL-6 release, and thus cooperatively promotes the pathogenesis of AP.
Source: Journal of Advanced Research - Category: Research Source Type: research