Wong Renee, Steenbergen Charles, Murphy Elizabeth
Cardiac Physiology Section, Systems Biology Center, NHLBI, NIH, Bethesda, MD 20892, USA.
Methods Mol Biol. 2012;810:235-42. doi: 10.1007/978-1-61779-382-0_15.
Opening of a large conductance channel in the inner mitochondrial membrane, known as the mitochondrial permeability transition (MPT) pore, has been shown to be a primary mediator of cell death in the heart subjected to ischemia-reperfusion injury. Inhibitors of the MPT have been shown to reduce cardiac ischemia-reperfusion injury. Furthermore, most cardioprotective strategies appear to reduce ischemic cell death either by reducing the triggers for the opening of the MPT, such as reducing calcium overload or reactive oxygen species, or by more direct inhibition of the MPT. This chapter focuses on key issues in the study of the MPT and provides some methods for measuring MPT opening in isolated mitochondria.
线粒体内膜中一种称为线粒体通透性转换(MPT)孔的大电导通道的开放,已被证明是遭受缺血再灌注损伤的心脏中细胞死亡的主要介质。MPT抑制剂已被证明可减轻心脏缺血再灌注损伤。此外,大多数心脏保护策略似乎通过减少MPT开放的触发因素(如减少钙超载或活性氧)或更直接地抑制MPT来减少缺血性细胞死亡。本章重点介绍MPT研究中的关键问题,并提供一些测量分离线粒体中MPT开放的方法。