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Mitochondrial dynamism and heart disease: changing shape and shaping change.

Dorn GW - EMBO Mol Med (2015)

Bottom Line: Nevertheless, proteins essential to mitochondrial network remodeling are abundant in adult hearts.Recent findings from cardiac-specific ablation of mitochondrial fission and fusion protein genes have revealed unexpected roles for mitochondrial dynamics factors in mitophagic mitochondrial quality control.This overview examines the clinical and experimental evidence for and against a meaningful role for the mitochondrial dynamism-quality control interactome in normal and diseased hearts.

View Article: PubMed Central - PubMed

Affiliation: Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA gdorn@dom.wustl.edu.

No MeSH data available.


Related in: MedlinePlus

The mitochondrial electron transport chain (ETC.) and its relationship to ROS productionEach of the inner mitochondrial membrane (IMM) ETC. enzymatic complexes is colored and indicated by their respective roman numerals (I-V). Electrons are transferred between complexes (dotted arrows), promoting proton (H+) transport (dashed arrows) from the matrix to the intermembrane space. Proton flow through ATP synthase (complex V) converts ADP to ATP. Normally, O2 is the terminal electron (e−) acceptor from complex IV. Electron leak from complexes I or III of damaged mitochondria can produce toxic reactive  and H2O2. Friedreich's ataxia is caused by mutations in frataxin that induces dysfunction in complexes I, II, and III. Mitochondrial DNA mutations can affect complexes I, III, IV, and V, but not complex II that is comprised entirely of nuclear-encoded proteins.
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fig02: The mitochondrial electron transport chain (ETC.) and its relationship to ROS productionEach of the inner mitochondrial membrane (IMM) ETC. enzymatic complexes is colored and indicated by their respective roman numerals (I-V). Electrons are transferred between complexes (dotted arrows), promoting proton (H+) transport (dashed arrows) from the matrix to the intermembrane space. Proton flow through ATP synthase (complex V) converts ADP to ATP. Normally, O2 is the terminal electron (e−) acceptor from complex IV. Electron leak from complexes I or III of damaged mitochondria can produce toxic reactive and H2O2. Friedreich's ataxia is caused by mutations in frataxin that induces dysfunction in complexes I, II, and III. Mitochondrial DNA mutations can affect complexes I, III, IV, and V, but not complex II that is comprised entirely of nuclear-encoded proteins.

Mentions: Mechanistic details of how mitochondria produce ATP and ROS are shown in Fig2.


Mitochondrial dynamism and heart disease: changing shape and shaping change.

Dorn GW - EMBO Mol Med (2015)

The mitochondrial electron transport chain (ETC.) and its relationship to ROS productionEach of the inner mitochondrial membrane (IMM) ETC. enzymatic complexes is colored and indicated by their respective roman numerals (I-V). Electrons are transferred between complexes (dotted arrows), promoting proton (H+) transport (dashed arrows) from the matrix to the intermembrane space. Proton flow through ATP synthase (complex V) converts ADP to ATP. Normally, O2 is the terminal electron (e−) acceptor from complex IV. Electron leak from complexes I or III of damaged mitochondria can produce toxic reactive  and H2O2. Friedreich's ataxia is caused by mutations in frataxin that induces dysfunction in complexes I, II, and III. Mitochondrial DNA mutations can affect complexes I, III, IV, and V, but not complex II that is comprised entirely of nuclear-encoded proteins.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4520653&req=5

fig02: The mitochondrial electron transport chain (ETC.) and its relationship to ROS productionEach of the inner mitochondrial membrane (IMM) ETC. enzymatic complexes is colored and indicated by their respective roman numerals (I-V). Electrons are transferred between complexes (dotted arrows), promoting proton (H+) transport (dashed arrows) from the matrix to the intermembrane space. Proton flow through ATP synthase (complex V) converts ADP to ATP. Normally, O2 is the terminal electron (e−) acceptor from complex IV. Electron leak from complexes I or III of damaged mitochondria can produce toxic reactive and H2O2. Friedreich's ataxia is caused by mutations in frataxin that induces dysfunction in complexes I, II, and III. Mitochondrial DNA mutations can affect complexes I, III, IV, and V, but not complex II that is comprised entirely of nuclear-encoded proteins.
Mentions: Mechanistic details of how mitochondria produce ATP and ROS are shown in Fig2.

Bottom Line: Nevertheless, proteins essential to mitochondrial network remodeling are abundant in adult hearts.Recent findings from cardiac-specific ablation of mitochondrial fission and fusion protein genes have revealed unexpected roles for mitochondrial dynamics factors in mitophagic mitochondrial quality control.This overview examines the clinical and experimental evidence for and against a meaningful role for the mitochondrial dynamism-quality control interactome in normal and diseased hearts.

View Article: PubMed Central - PubMed

Affiliation: Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA gdorn@dom.wustl.edu.

No MeSH data available.


Related in: MedlinePlus