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运动通过通过M调节内分泌网膜应激和线粒细胞衰变来减轻心肌缺血-再输液损伤
Wei Chen1,2, Mei Ma1, Yinping Song1
1Institute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi'an, China.
Antioxidants & redox signaling
|June 9, 2023
概括
运动通过M2乙胆受体 (M2AChR) 激活了副交感神经,以减少内分泌网膜应激 (ERS) 和髓,防止心脏缺血 - 反损伤.
科学领域:
- 心血管科学 心血管科学
- 分子生物学分子生物学
- 运动生理学 运动生理学
背景情况:
- 运动通过调节心脏功能,有利于心血管健康.
- 心脏神经上的M2乙胆受体 (M2AChR) 与心血管疾病有关.
- 细胞内膜网膜应激 (ERS) 和线粒会导致心肌损伤.
研究的目的:
- 调查运动是否通过M2AChR调节ESR和线粒细胞衰变,以减轻心肌缺血-再输液 (I/R) 损伤.
- 为了阐明底层的分子机制.
主要方法:
- 使用I/R损伤的老鼠模型.
- 评估了副交感神经功能和M2AChR表达.
- 分析了与ERS,线粒和亡相关的蛋白质表达.
- 使用H9C2心肌细胞与缺氧/复氧化 (H/R) 和M2AChR抑制剂进行的细胞研究.
主要成果:
- 运动增强了I/R大鼠的副交感活动和M2AChR表达.
- 运动通过调节MFN2,Drp1,Chop,PINK1/Parkin和PERK/eIF2α/ATF4通路来降低了ERS,线粒和亡.
- 在心肌细胞中,AICAR治疗降低了H/R诱导的ERS.
- 在H/R细胞中,M2AChR抑制加剧了ERS和PERK/eIF2α/ATF4通路的激活.
结论:
- 运动激活了副交感状态,通过M2AChR抑制心肌髓和ERS.
- 这种机制减少了心肌亡,并防止I / R损伤,改善心脏功能.
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