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Caspase inhibition prevents cardiac dysfunction and heart apoptosis in a rat model of sepsis.

Caspase inhibition prevents cardiac dysfunction and heart apoptosis in a rat model of sepsis.

http://www.wikidata.org/entity/Q32033049

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Sepsis-induced Cardiac Mitochondrial Damage and Potential Therapeutic Interventions in the Elderly Pathophysiology of sepsis-induced myocardial dysfunction Over-expression of calpastatin inhibits calpain activation and attenuates myocardial dysfunction during endotoxaemia Protective effect of caspase inhibition on compression-induced muscle damage Effects of a caspase and a calpain inhibitor on resting energy expenditures in normal and hypermetabolic rats: a pilot study Critical care medicine in AJRCCM 2001.The effects of lazaroid U-74389G in a rat sepsis model.Recent developments in the treatment of sepsis.Bench to bedside: the role of mitochondrial medicine in the pathogenesis and treatment of cellular injury.β₁-adrenoceptor stimulation promotes LPS-induced cardiomyocyte apoptosis through activating PKA and enhancing CaMKII and IκBα phosphorylation.Sepsis-induced cardiomyopathy.Inhibition of caspase mediated apoptosis restores muscle function after crush injury in rat skeletal muscle Caspases: potential targets for regulating cell death.17-DMAG, an HSP90 Inhibitor, Ameliorates Multiple Organ Dysfunction Syndrome via Induction of HSP70 in Endotoxemic Rats.Ecto-5'-nucleotidase (CD73) decreases mortality and organ injury in sepsis.Role of apoptosis in ventricular remodeling.Effect of nerve growth factor and its transforming tyrosine kinase protein and low-affinity nerve growth factor receptors on apoptosis of notochordal cells.Apoptosis and caspases regulate death and inflammation in sepsis.Circulating pro-apoptotic mediators in burn septic acute renal failure.Inhibition of MicroRNA 195 Prevents Apoptosis and Multiple-Organ Injury in Mouse Models of Sepsis.Role of Kir6.2 subunits of ATP-sensitive potassium channels in endotoxemia-induced cardiac dysfunction.Molecular events in the cardiomyopathy of sepsis.Severe bacteremia results in a loss of hepatic bacterial clearance Infarction induced myocardial apoptosis and ARC activation Cardiac Electrical and Structural Changes During Bacterial Infection: An Instructive Model to Study Cardiac Dysfunction in Sepsis.MitoQ administration prevents endotoxin-induced cardiac dysfunction.Inhibition of miR-155 Protects Against LPS-induced Cardiac Dysfunction and Apoptosis in Mice.Caspase and calpain activation both contribute to sepsis-induced diaphragmatic weakness.Noncleavable poly(ADP-ribose) polymerase-1 regulates the inflammation response in mice.Use of zebrafish apoptosis assays for preclinical drug discovery.Enhanced Glycolytic Metabolism Contributes to Cardiac Dysfunction in Polymicrobial Sepsis.MicroRNA-125b Prevents Cardiac Dysfunction in Polymicrobial Sepsis by Targeting TRAF6-Mediated Nuclear Factor κB Activation and p53-Mediated Apoptotic Signaling.Melatonin attenuates sepsis-induced cardiac dysfunction via a PI3K/Akt-dependent mechanism.Eicosapentaenoic acid preserves diaphragm force generation following endotoxin administration.Polyethylene glycol-superoxide dismutase prevents endotoxin-induced cardiac dysfunction.Contractile response of norepinephrine is modulated by caspase-3 in adult rat ventricular myocytes isolated from septic rat heart Differential effects of caspase inhibitors on endotoxin-induced myocardial dysfunction and heart apoptosis.Protective effects of cyclosporin A from endotoxin-induced myocardial dysfunction and apoptosis in rats.The extrinsic caspase pathway modulates endotoxin-induced diaphragm contractile dysfunction.Apoptosis inhibition in P. aeruginosa-induced lung injury influences lung fluid balance.

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P2860

Caspase inhibition prevents cardiac dysfunction and heart apoptosis in a rat model of sepsis.

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AJRCCM.163.1.2003109

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American Journal of Respiratory and Critical Care Medicine

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Caspase inhibition prevents ca ...... tosis in a rat model of sepsis

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P2093

Chopin C

http://www.w3.org/2001/XMLSchema#string

Fauvel H

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Formstecher P

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Nevière R

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P2860

Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

Caspase activation without death.

Tumor necrosis factor-alpha gene and protein expression in adult feline myocardium after endotoxin administration.

Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart.

A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance

Apoptotic pathways: the roads to ruin.

Endotoxin and tumor necrosis factor challenges in dogs simulate the cardiovascular profile of human septic shock.

Apoptosis in heart failure: release of cytochrome c from mitochondria and activation of caspase-3 in human cardiomyopathy.

Stimulation of CD95 (Fas) blocks T lymphocyte calcium channels through sphingomyelinase and sphingolipids.

Tumor necrosis factor alpha-induced apoptosis in cardiac myocytes. Involvement of the sphingolipid signaling cascade in cardiac cell death.

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