Difference between revisions of "Larche 2006 J Am Coll Cardiol"
Beno Marija (talk | contribs) Β |
|||
(10 intermediate revisions by 6 users not shown) | |||
Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, Chopin C, Neviere R (2006)Β Inhibition of mitochondrial permeability transition prevents sepsis-induced myocardial dysfunction and mortality. J | |title=Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, Chopin C, Neviere R (2006)Β Inhibition of mitochondrial permeability transition prevents sepsis-induced myocardial dysfunction and mortality. J Am Coll Cardiol 48:377-85. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16843190 PMID: 16843190] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/16843190 PMID: 16843190 Open Access] | ||
|authors=Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, Chopin C, Neviere R | |authors=Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, Chopin C, Neviere R | ||
|year=2006 | |year=2006 | ||
|journal=J | |journal=J Am Coll Cardiol | ||
|abstract=OBJECTIVES The purpose of this study was to test whether mitochondrial dysfunction is causative of sepsis sequelae, a mouse model of peritonitis sepsis induced by cecal ligation and perforation. Inhibition of mitochondrial permeability transition was achieved by means of pharmacological drugs and overexpression of the antiapoptotic protein B-cell leukemia (Bcl)-2. | |abstract=OBJECTIVES The purpose of this study was to test whether mitochondrial dysfunction is causative of sepsis sequelae, a mouse model of peritonitis sepsis induced by cecal ligation and perforation. Inhibition of mitochondrial permeability transition was achieved by means of pharmacological drugs and overexpression of the antiapoptotic protein B-cell leukemia (Bcl)-2. | ||
Line 15: | Line 15: | ||
CONCLUSIONS Our study provides strong evidence that mitochondrial permeability transition plays a critical role in septic organ dysfunction. These studies demonstrate that mitochondrial dysfunction in sepsis is causative rather than epiphenomenal and relevant in terms of vital organ function and outcome. | CONCLUSIONS Our study provides strong evidence that mitochondrial permeability transition plays a critical role in septic organ dysfunction. These studies demonstrate that mitochondrial dysfunction in sepsis is causative rather than epiphenomenal and relevant in terms of vital organ function and outcome. | ||
Regarding the critical role of heart failure in the pathophysiology of septic shock, our study also indicates a potentially new therapeutic approach for treatment of sepsis syndrome. | Regarding the critical role of heart failure in the pathophysiology of septic shock, our study also indicates a potentially new therapeutic approach for treatment of sepsis syndrome. | ||
|mipnetlab= | |mipnetlab=FR Lille Neviere R, FR Lille Lancel Steve | ||
|discipline=Biomedicine, Pharmacology; Biotechnology | |discipline=Biomedicine, Pharmacology; Biotechnology | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Human, Mouse | |||
|tissues=Heart | |||
|preparations=Intact cells, Isolated mitochondria | |||
|injuries=Mitochondrial disease | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Biomedicine, Pharmacology; Biotechnology | |discipline=Biomedicine, Pharmacology; Biotechnology | ||
}} | }} |
Latest revision as of 11:50, 22 December 2020
Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, Chopin C, Neviere R (2006) Inhibition of mitochondrial permeability transition prevents sepsis-induced myocardial dysfunction and mortality. J Am Coll Cardiol 48:377-85. |
Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, Chopin C, Neviere R (2006) J Am Coll Cardiol
Abstract: OBJECTIVES The purpose of this study was to test whether mitochondrial dysfunction is causative of sepsis sequelae, a mouse model of peritonitis sepsis induced by cecal ligation and perforation. Inhibition of mitochondrial permeability transition was achieved by means of pharmacological drugs and overexpression of the antiapoptotic protein B-cell leukemia (Bcl)-2.
BACKGROUND Sepsis is the leading cause of death in critically ill patients and the predominant cause of multiple organ failure. Although precise mechanisms by which sepsis leads to multiple organ dysfunction are unknown, growing evidence suggests that perturbations of key mitochondrial functions, including adenosine triphosphate production, Ca2+ homeostasis, oxygen-derived free radical production, and permeability transition, might be involved in sepsis pathophysiology.
METHODS Heart and lung functions were evaluated respectively by means of isolated heart preparation, bronchoalveolar lavage fluid protein concentration, lung wet/dry weight ratio, lung homogenate myeloperoxidase activity, and histopathologic grading. Respiratory fluxes, calcium uptake, and membrane potential were evaluated in isolated heart mitochondria.
RESULTS Peritonitis sepsis induced multiple organ dysfunction, mitochondrial abnormalities, and increased mortality rate, which were reduced by pharmacological inhibition of mitochondrial transition by cyclosporine derivatives and mitochondrial Bcl-2 overexpression.
CONCLUSIONS Our study provides strong evidence that mitochondrial permeability transition plays a critical role in septic organ dysfunction. These studies demonstrate that mitochondrial dysfunction in sepsis is causative rather than epiphenomenal and relevant in terms of vital organ function and outcome. Regarding the critical role of heart failure in the pathophysiology of septic shock, our study also indicates a potentially new therapeutic approach for treatment of sepsis syndrome.
β’ O2k-Network Lab: FR Lille Neviere R, FR Lille Lancel Steve
Labels:
Stress:Mitochondrial disease Organism: Human, Mouse Tissue;cell: Heart Preparation: Intact cells, Isolated mitochondria
Coupling state: OXPHOS
HRR: Oxygraph-2k