线粒体融合
神经退行性变
线粒体
细胞器
细胞生物学
生物
线粒体分裂
细胞凋亡
程序性细胞死亡
神经科学
线粒体DNA
遗传学
基因
医学
病理
疾病
作者
M Wasilewski,Luca Scorrano
标识
DOI:10.1016/j.tem.2009.03.007
摘要
Mitochondria are key organelles in conversion of energy, regulation of cellular signaling and amplification of programmed cell death. The anatomy of the organelle matches this functional versatility in complexity and is modulated by the concerted action of proteins that impinge on its fusion–fission equilibrium. A growing body of evidence implicates changes in mitochondrial shape in the progression of apoptosis and, therefore, proteins governing such changes are likely candidates for involvement in pathogenetic mechanisms in neurodegeneration and cancer. Here, we discuss the recent advancements in our knowledge about the machinery that regulates mitochondrial shape and on the role of molecular mechanisms controlling mitochondrial morphology during cell death. Mitochondria are key organelles in conversion of energy, regulation of cellular signaling and amplification of programmed cell death. The anatomy of the organelle matches this functional versatility in complexity and is modulated by the concerted action of proteins that impinge on its fusion–fission equilibrium. A growing body of evidence implicates changes in mitochondrial shape in the progression of apoptosis and, therefore, proteins governing such changes are likely candidates for involvement in pathogenetic mechanisms in neurodegeneration and cancer. Here, we discuss the recent advancements in our knowledge about the machinery that regulates mitochondrial shape and on the role of molecular mechanisms controlling mitochondrial morphology during cell death.
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