TRPV6-mediated Store-operated Ca²⁺ Entry Participates in Pancreatic Acinar Cell Injury During Acute Pancreatitis.

ABSTRACT:

Background & aims

Suppressing toxic Ca²⁺ accumulation in pancreatic acinar cells (PACs) is the central therapeutic strategy of acute pancreatitis (AP). Store-operated Ca²⁺ entry (SOCE) represents an important mechanism promoting Ca²⁺ overload, which remains incompletely understood in AP. Transient receptor potential vanilloid 6 (TRPV6) is an ion channel highly selective to Ca²⁺, and its role in PACs or AP onset remains largely unknown.

Methods

We utilized human and mouse pancreata for TRPV6 expression using RNAscope and PACs for electrophysical currents and Ca²⁺ signals identification. Following RNA sequencing, we examined the interaction between TRPV6 and stromal interaction molecule 1 (STIM1) at the junctions between t

SUBMITTER: Han C 

PROVIDER: S-EPMC12553069 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature