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运动前调节通过激活NRF2减轻TAC诱导的心脏缩和心肌损伤

Lihua Ni¹, Binger Lu², Guangquan Peng³

¹Department of Pharmacology, Shantou University Medical College, Shantou, 515041, China; Clinical Research Center, Shantou Central Hospital, Shantou, 515041, China.

Free radical biology & medicine

|July 18, 2025

概括

运动预先调节通过激活SIRT1-NRF2通路来保护心脏免受压力过载. 这种激活减少了氧化应激,减轻了小鼠的心脏缩和功能障碍.

科学领域:

心血管生物学心血管生物学
运动生理学运动生理学
分子心脏病学分子心脏病学

背景情况:

病理性心脏缩和心力衰竭是显著的临床问题.
运动对心脏压力的保护机制仍然不完全理解.

研究的目的:

研究SIRT1-NRF2通路在运动中介心脏保护中的作用.
阐明运动可以防止压力过载下心脏功能障碍的机制.

主要方法:

利用横向大动脉收缩 (TAC) 鼠标模型来模拟压力过载.
在TAC手术前给小鼠进行运动预调.
评估心脏缩,纤维化,缩功能和氧化应激标志物.
雇佣了Nrf2淘汰 (Nrf2-KO) 的小鼠来确认Nrf2激活的必要性.

主要成果:

运动预先条件显著减弱TAC诱导的心脏缩,纤维化和缩功能障碍.
这些保护作用与SIRT1-NRF2通路的激活和减少氧化应激有很强的相关性.
Nrf2 缺乏完全消除了运动的有益影响,消除了心脏参数和氧化应激的改善.

结论:

运动预先调节可以显著地保护心脏,防止压力过重引起的心脏缩和功能障碍.
保护作用主要由Nrf2激活介导,该激活抑制氧化应激.
Nrf2是运动诱导心脏益处的关键分子标.

关键词:

运动前置条件 - 运动前置条件心脏衰竭是因为心脏衰竭.Nrf2 没有任何问题.氧化应激是一种氧化应激.

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