FIGURE 1 Mitochondrial dysfunction affects diverse cellular processes that can culminate in cell death.
From the following article:
Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis
Claire Henchcliffe and M Flint Beal
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Figure 1. Mitochondrial dysfunction affects diverse cellular processes that can culminate in cell death.
Mitochondrial dysfunction affects a number of cellular pathways, leading to damage of intracellular components and to cell death. Abnormal metabolic function, abnormal morphology, and impaired fission–fusion balance have all been observed in mitochondria in at least some forms of Parkinson disease. Mitochondria are a major source of free radicals in the cell, resulting in oxidative stress, but mitochondria are also integral to the oxidative stress response. Increased oxidative stress can lead to impaired function of the UPS, thereby further affecting cell survival. Mitochondria also sequester calcium when intracellular calcium levels rise during the excitotoxic process. The threshold for excitotoxicity might decrease if mitochondrial ATP production is impaired. Mitochondria also have a pivotal role in apoptotic cell death. Mitochondrial release of cytochrome c and other 'pro-apoptotic factors', such as AIF, into the cytoplasm triggers a cascade of events, culminating in cell death. Abbreviations: AIF, apoptosis-initiating factor; UPS, ubiquitin–proteasomal system.
