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作 者:曹伟琪 郭晓英 Cao Weiqi;Guo Xiaoying(Department of Environmental Health,School of Public Health,China Medical University,Shenyang 110122,China)
机构地区:[1]中国医科大学公共卫生学院环境卫生学教研室,沈阳110122
出 处:《中华地方病学杂志》2023年第11期933-937,共5页Chinese Journal of Endemiology
基 金:国家自然科学基金(82073497);"中国医科大学大学生创新创业训练计划"资助项目(S202210159004)。
摘 要:氟是一种广泛存在于自然界的重要元素。人体摄入适量的氟可以有效地预防龋齿,促进骨骼和牙齿发育。但长期过量氟摄入可导致氟中毒,引起氟斑牙和氟骨症。此外,氟中毒还可以损害心肌的结构和功能,进而影响人体健康。然而,目前氟中毒对心肌损害的机制尚未完全阐明,因此深入探讨其相关机制对氟中毒的防治意义重大。细胞凋亡、Ca^(2+)通道、氧化应激以及相关细胞因子的失衡均在氟中毒所致的心肌细胞损害中起重要作用。本文主要综述了氟中毒对心肌的损害作用及相关分子机制的研究进展,并对未来研究方向提出了展望。Fluorine is an essential element widespread in nature.Appropriate concentration of fluorine is beneficial to prevent dental caries and promote the development of bones and teeth.But long-term excessive intake of fluorine can lead to fluorosis,causing dental fluorosis and skeletal fluorosis.In addition,fluorosis can also damage the structure and function of myocardium,thereby affecting human health.However,the underlying mechanism has not been thoroughly elucidated,so it is of great significance to explore its related mechanism for prevention and treatment of fluorosis.Apoptosis,Ca^(2+)channel,oxidative stress,and imbalance of related cytokines all play important roles in myocardium injury caused by fluorosis.This article mainly reviews the effects of fluorosis on myocardium and its related molecular mechanisms,and proposes prospects for future research directions.
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