Regulation of Mitochondrial Dynamics and Cell Fate

Though the mitochondrion was initially identified as a key organelle essentially required for energy production and oxidative metabolism, there is considerable evidence that mitochondria are intimately involved in regulating vital cellular processes, such as programmed cell death, proliferation and...

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Bibliographic Details
Published in:Circulation Journal 2014, Vol.78(4), pp.803-810
Main Authors: Dhingra, Rimpy, Kirshenbaum, Lorrie A.
Format: Article
Language:English
Subjects:
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Animals
Cardiovascular Diseases - genetics
Cardiovascular Diseases - metabolism
Cardiovascular Diseases - pathology
Cell death
Drp1
Dynamins - immunology
Dynamins - metabolism
Fission
Fusion
Humans
Mitochondria - genetics
Mitochondria - metabolism
Mitochondria - pathology
Mitochondrial Dynamics - genetics
Mitochondrial Membrane Transport Proteins - genetics
Mitochondrial Membrane Transport Proteins - metabolism
Mitochondrion
Parkinson Disease - genetics
Parkinson Disease - metabolism
Parkinson Disease - pathology
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Summary:Though the mitochondrion was initially identified as a key organelle essentially required for energy production and oxidative metabolism, there is considerable evidence that mitochondria are intimately involved in regulating vital cellular processes, such as programmed cell death, proliferation and autophagy. Discovery of mitochondrial “shaping proteins” (Dynamin-related protein (Drp), mitofusins (Mfn) etc.) has revealed that mitochondria are highly dynamic organelles continually changing morphology by fission and fusion processes. Several human pathologies, including cancer, Parkinson’s disease, Alzheimer’s disease and cardiovascular diseases, have been linked to abnormalities in proteins that govern mitochondrial fission or fusion respectively. Notably, in the context of the heart, defects in mitochondrial dynamics resulting in too many fused and/or fragmented mitochondria have been associated with impaired cardiac development, autophagy, and contractile dysfunction. Understanding the mechanisms that govern mitochondrial fission/fusion is paramount in developing new treatment strategies for human diseases in which defects in fission or fusion is the primary underlying defect. Here, we provide a comprehensive overview of the cellular targets and molecular signaling pathways that govern mitochondrial dynamics under normal and disease conditions.  (Circ J 2014; 78: 803–810)
ISSN:1346-9843
1347-4820
DOI:10.1253/circj.CJ-14-0240