Abstract
Excessive alcohol intake can induce gut barrier dysfunction, leading to endotoxemia and systemic inflammation. The molecular mechanism resulting in the alcohol-induced Ca2+ increase responsible for gut barrier dysfunction has remained elusive. TRPV6, a member of the transient receptor potential vanilloid subfamily, is unique in its high selectivity for Ca2+ and involvement in maintaining Ca2+ homeostasis. Interestingly, TRPV6 is highly expressed in the apical membrane of the intestinal epithelium.
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