Abstract
findings strongly suggest that GPR30 is a novel, selective target for the prevention and the treatment of estrogen-induced cholesterol gallstones. Conclusions: GPR30 is also involved in estrogen-dependent lithogenic actions, working independently from ERα, as both GPR30 and ERα can work through different pathways to promote the formation of estrogen-induced gallstones. Distinguishing the lithogenic actions of GPR30 from ERα and further investigating how estrogen produces lithogenic actions via GPR30 may help better understand the molecular mechanisms behind the formation of cholesterol gallstones induced by estrogen.
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