Difference between revisions of "Montaigne 2011 Mitochondrion"
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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 | |mipnetlab=FR Lille Neviere R, FR Lille Lancel Steve | ||
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{{Labeling | {{Labeling | ||
Latest revision as of 11:48, 22 December 2020
| 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 11:22-6. |
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.
• O2k-Network Lab: FR Lille Neviere R, FR Lille Lancel Steve
Labels:
Organism: Human
Tissue;cell: Heart
Preparation: Isolated mitochondria
HRR: Oxygraph-2k
TPP: WPI electrode
