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心肌细胞过氧体增殖器激活受体α通过改善线粒体功能来预防败血性心肌病

Xin-Xin Zhu¹, Xia Wang¹, Shi-Yu Jiao¹

¹Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University; Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Key Laboratory of Metabolic Disorder-Related Cardiovascular Diseases, Beijing, 100069, China.

Acta pharmacologica Sinica

|June 16, 2023

概括

心肌细胞PPARα通过改善线粒体功能和脂肪酸代谢来预防败血性心肌病. 这突出了心肌细胞PPARα作为败血症引起的心脏病的潜在治疗点.

科学领域:

心血管生物学心血管生物学
线粒体医学线粒体医学
分子心脏病学分子心脏病学

背景情况:

败血症引起的心脏功能障碍是多器官衰竭的主要原因之一.
线粒体功能障碍,线粒体和亡是败血性心肌病的关键.
在败血症中准线粒体功能的治疗策略仍未得到充分探索.

研究的目的:

调查过氧体增殖器激活受体α (PPARα) 在心肌细胞静止在败血症期间的作用.
确定PPARα对脂聚糖 (LPS) 诱导的心脏功能障碍的细胞特异性保护作用.
探索PPARα作为败血性心肌病的潜在治疗点.

主要方法:

对败血症小鼠心脏的转录组分析发现了PPAR信号的减少.
使用心肌细胞特异性Ppara缺陷 (Ppara^ΔCM) 和骨髓特异性Ppara缺陷 (Ppara^ΔMac) 的小鼠接受LPS治疗.
评估心脏功能,线粒体完整性,ATP含量,酶活动,蛋白质水平和炎症信号通路.

主要成果:

心肌细胞特异性Ppara缺陷加剧了LPS诱导的心脏功能障碍和线粒体损伤.
心肌细胞中的PPARα缺乏会损害脂肪酸代谢,增加线粒,并促进亡.
PPARα激动剂WY14643和自抑制剂3-MA改善了败血性心肌病.

结论:

心肌细胞PPARα,而不是骨髓质PPARα,可以预防败血性心肌病.
在败血症期间,PPARα可以改善心脏线粒体功能和脂肪酸代谢.
向心肌细胞PPARα代表了感染性心脏病的一个有前途的治疗策略.

关键词:

心脏功能障碍的心脏功能障碍这是一种炎症炎症炎症炎症.线粒体功能障碍线粒体功能障碍线粒细胞衰变 (mitophagy) 是一种神经衰变的过程.过氧体增殖器激活受体α的受体.这是一种血症.

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