磷酸肌酸
线粒体
肌酸激酶
胞浆
线粒体通透性转换孔
细胞生物学
氧化磷酸化
三磷酸腺苷
生物化学
氧化应激
生物
肌酸
生物物理学
化学
细胞凋亡
程序性细胞死亡
能量代谢
酶
内分泌学
作者
Uwe Schlattner,Małgorzata Tokarska-Schlattner,Theo Wallimann
标识
DOI:10.1016/j.bbadis.2005.09.004
摘要
Mitochondrial creatine kinase (MtCK), together with cytosolic creatine kinase isoenzymes and the highly diffusible CK reaction product, phosphocreatine, provide a temporal and spatial energy buffer to maintain cellular energy homeostasis. Mitochondrial proteolipid complexes containing MtCK form microcompartments that are involved in channeling energy in form of phosphocreatine rather than ATP into the cytosol. Under situations of compromised cellular energy state, which are often linked to ischemia, oxidative stress and calcium overload, two characteristics of mitochondrial creatine kinase are particularly relevant: its exquisite susceptibility to oxidative modifications and the compensatory up-regulation of its gene expression, in some cases leading to accumulation of crystalline MtCK inclusion bodies in mitochondria that are the clinical hallmarks for mitochondrial cytopathies. Both of these events may either impair or reinforce, respectively, the functions of mitochondrial MtCK complexes in cellular energy supply and protection of mitochondria form the so-called permeability transition leading to apoptosis or necrosis.
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