Difference between revisions of "Montaigne 2011 Mitochondrion"
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{{Publication | {{Publication | ||
|title=Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R (2011) Doxorubicin induces mitochondrial permeability transition and contractile dysfunction in the human myocardium | |title=Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R (2011) Doxorubicin induces mitochondrial permeability transition and contractile dysfunction in the human myocardium. Mitochondrion 11(1):22-26. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20599629 PMID:20599629] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/20599629 PMID:20599629] | ||
|authors=Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R | |authors=Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R | ||
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|journal=Mitochondrion | |journal=Mitochondrion | ||
|abstract=In human atrial trabeculae, we examined the effects of doxorubicin on the isometric force of contraction, mitochondrial respiration, membrane potential and calcium retention capacity. Compared with untreated controls, doxorubicin induced contractile dysfunction and depression of mitochondrial respiration. Mitochondria isolated from doxorubicin-treated human atrial trabeculae displayed reduced transmembrane potential and calcium retention capacity. Cyclosporine A, a mitochondrial membrane transition pore opening blocker, prevented mitochondrial dysfunction and impaired contractile performance induced by doxorubicin. The study suggests that a mitochondrial membrane transition pore opening is involved in the development of doxorubicin cardiotoxicity in human hearts. | |abstract=In human atrial trabeculae, we examined the effects of doxorubicin on the isometric force of contraction, mitochondrial respiration, membrane potential and calcium retention capacity. Compared with untreated controls, doxorubicin induced contractile dysfunction and depression of mitochondrial respiration. Mitochondria isolated from doxorubicin-treated human atrial trabeculae displayed reduced transmembrane potential and calcium retention capacity. Cyclosporine A, a mitochondrial membrane transition pore opening blocker, prevented mitochondrial dysfunction and impaired contractile performance induced by doxorubicin. The study suggests that a mitochondrial membrane transition pore opening is involved in the development of doxorubicin cardiotoxicity in human hearts. | ||
|mipnetlab=FR Lille Neviere R, Â | |mipnetlab=FR Lille Neviere R, | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 17:48, 13 October 2011
| Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R (2011) Doxorubicin induces mitochondrial permeability transition and contractile dysfunction in the human myocardium. Mitochondrion 11(1):22-26. |
Montaigne D, Marechal X, Preau S, Baccouch R, Modine T, Fayad G, Lancel S, Neviere R (2011) Mitochondrion
Abstract: In human atrial trabeculae, we examined the effects of doxorubicin on the isometric force of contraction, mitochondrial respiration, membrane potential and calcium retention capacity. Compared with untreated controls, doxorubicin induced contractile dysfunction and depression of mitochondrial respiration. Mitochondria isolated from doxorubicin-treated human atrial trabeculae displayed reduced transmembrane potential and calcium retention capacity. Cyclosporine A, a mitochondrial membrane transition pore opening blocker, prevented mitochondrial dysfunction and impaired contractile performance induced by doxorubicin. The study suggests that a mitochondrial membrane transition pore opening is involved in the development of doxorubicin cardiotoxicity in human hearts.
âą O2k-Network Lab: FR Lille Neviere R
Labels:
Organism: Human
Tissue;cell: Cardiac Muscle"Cardiac Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Coupling; Membrane Potential"Coupling; Membrane Potential" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
