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. 2012 Jun;139(6):455-63.
doi: 10.1085/jgp.201210771.

Perspectives on: SGP symposium on mitochondrial physiology and medicine: what comes first, misshape or dysfunction? The view from metabolic excess

Chad A Galloway  1 , Yisang Yoon
Affiliations

Perspectives on: SGP symposium on mitochondrial physiology and medicine: what comes first, misshape or dysfunction? The view from metabolic excess

Chad A Galloway et al. J Gen Physiol. 2012 Jun.
No abstract available

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Figures

Figure 1.
Figure 1.
Mitochondrial morphology and function in metabolic excess. Increased metabolic input in the form of high glucose and/or fat (HG/HF) provides an increased entry of reducing equivalents into the ETC resulting in enhanced ΔΨm, favorable for electron slippage and ROS production. Metabolic signaling may alter mitochondrial morphology in HG/HF conditions. Altered mitochondrial morphology under metabolic excess plays a role in ROS production and subsequent mitochondrial dysfunction. Conversely, ROS inside mitochondria causes mitochondrial dysfunction, which may affect mitochondrial morphology. Accumulating damage inside of mitochondria through ROS progressively causes irreversible mitochondrial dysfunction for a new exacerbating cycle of ROS and mitochondrial dysfunction. Apoptosis and dysregulation of mitophagy are accompanied in the metabolic insult conditions, which also interface with mitochondrial morphology change.
Figure 2.
Figure 2.
Morphological control to restore mitochondrial function in metabolic insult. Proper maintenance of mitochondrial morphology ensures proper bioenergetic activities and vice versa. Because of a reciprocal relationship between mitochondrial form and function, dysregulation of either mitochondrial morphology or function in metabolic excess causes a cycle of mitochondrial dysfunction and deformation, resulting in metabolic disease. Morphological intervention could put the brake on this vicious cycle and restore normal form of mitochondria, which leads to the recovery of normal function.
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