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药理上的SERCA激活限制了饮食引起的脂肪肝炎,并恢复了小鼠的肝脏代谢功能

Tomasz K Bednarski¹, Mohsin Rahim¹, Clinton M Hasenour¹

¹Department of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, TN, USA.

Journal of lipid research

|May 10, 2024

概括

萨尔科/ER Ca2+-ATPase (SERCA) 的药理活性改善了小鼠的代谢功能障碍相关的脂肪性肝病. 恢复SERCA功能限制了内质网膜压力和线粒体功能障碍,改善了肝脏健康和代谢参数.

科学领域:

肝病学肝病学是一种肝病学.
代谢疾病代谢疾病
细胞生物学细胞生物学

背景情况:

与代谢功能障碍相关的脂肪性肝病 (MASLD) 是一种具有重大健康风险的普遍疾病.
肝细胞中的脂肪酸过载会破坏的平衡,从而导致细胞内网膜 (ER) 压力,线粒体功能障碍,炎症和亡.
在肥胖症中损害的sarco/ER Ca2+-ATPase (SERCA) 功能损害了细胞内调节.

研究的目的:

调查恢复SERCA活性是否可以改善小鼠的饮食诱导的脂肪肝炎和代谢功能障碍.
确定SERCA激活对ER压力,线粒体功能和肝脏炎症通路的影响.

主要方法:

野生型和Mc4r-/-型小鼠被食西方饮食 (WD) 8周.
CDN1163是一种SERCA激活剂,给了一组WD养的小鼠.
评估肝脏组织学,葡萄糖耐受性,胰岛素敏感性,基因表达 (抗氧化剂,氧化应激,ER应激,线粒体呼吸) 和代谢流量.

主要成果:

CDN1163治疗减少了肝纤维化,炎症,并改善了MASLD的组织学标志物.
激活SERCA恢复了葡萄糖耐受性和胰岛素敏感性.
CDN1163降低了氧化和ER压力标志物,增加了抗氧化酶表达,并改变了肝脏代谢途径,包括酸循环流量.

结论:

药理上SERCA激活有效地限制了小鼠在WD养中诱导的MASLD的进展.
恢复SERCA活动可以减轻ER压力和线粒体功能障碍,为MASLD和相关代谢障碍提供潜在的治疗策略.

关键词:

和是最重要的.酸循环的酸周期肝脏病学肝脏病学与代谢功能障碍相关的脂肪肝炎.与代谢功能障碍相关的脂肪性肝病.代谢流量分析的代谢流量分析.代谢代谢代谢代谢非酒精性脂肪性肝病是什么?没有酒精含量的型肝炎.多不和脂肪酸多不和脂肪酸酸盐循环循环使用石灰运输ATPase的sarcoplasmic/endoplasmic网膜中的一个.

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