摘要:
在运动等生理性刺激或甲亢、高血压等病理性刺激会诱发心肌发生生理性或病理性心肌肥厚,研究证实众多细胞氧化还原失衡和/或线粒体功能紊乱是心肌肥厚过程发生和/或发展的重要机制之一。本文系统、深入地综述了心脏反应氧簇的产生和其作用于相应的靶向蛋白的信号分子及其调控机制。
Abstract: Redundancy redox molecular and mitochondrial dysfunction are one of the important mechanisms of physiological or pathological cardiac hypertrophy induced by exercise or hyperthyroidism, hyper- tension and other pathological stimulation, so we review reaction oxygen species generation and its role in the corresponding target signal molecule protein and its regulation mechanism in heart.