Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts. - Wikidata - awgldk - TriplyDB

Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts.

Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts.

http://www.wikidata.org/entity/Q46939197

about

Excitation-contraction coupling in ventricular myocytes is enhanced by paracrine signaling from mesenchymal stem cells.Basal bioenergetic abnormalities in skeletal muscle from ryanodine receptor malignant hyperthermia-susceptible R163C knock-in mice.Ischemia/reperfusion injury and cardioprotective mechanisms: Role of mitochondria and reactive oxygen species A novel role for mitochondrial sphingosine-1-phosphate produced by sphingosine kinase-2 in PTP-mediated cell survival during cardioprotection.Blockade of electron transport before ischemia protects mitochondria and decreases myocardial injury during reperfusion in aged rat hearts A soluble receptor for advanced glycation end-products inhibits hypoxia/reoxygenation-induced apoptosis in rat cardiomyocytes via the mitochondrial pathway.Protective ischaemia in patients: preconditioning and postconditioning.The Citrus Flavanone Naringenin Protects Myocardial Cells against Age-Associated Damage.Postconditioning and protection from reperfusion injury: where do we stand? Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology.There is more to life than revascularization: therapeutic targeting of myocardial ischemia/reperfusion injury.Postconditioning: from the bench to bedside.Diabetic inhibition of preconditioning- and postconditioning-mediated myocardial protection against ischemia/reperfusion injury.Redox balance and cardioprotection.Cardiac aquaporins.Cardiomyocyte changes in the metabolic syndrome and implications for endogeneous protective strategies.The role of HIFs in ischemia-reperfusion injury.Desflurane-induced and ischaemic postconditioning against myocardial infarction are mediated by Pim-1 kinase.Diazoxide postconditioning induces mitochondrial protein S-nitrosylation and a redox-sensitive mitochondrial phosphorylation/translocation of RISK elements: no role for SAFE.Minor Changes in Core Temperature Prior to Cardiac Arrest Influence Outcomes: An Experimental Study.Fast therapeutic hypothermia prevents post-cardiac arrest syndrome through cyclophilin D-mediated mitochondrial permeability transition inhibition.Mitochondria in Cardiac Postconditioning.

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P2860

Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts.

http://www.wikidata.org/entity/Q46939197

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年學術文章

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2007年學術文章

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name

Increased mitochondrial calciu ...... ut not preconditioned) hearts.

@en

Increased mitochondrial calciu ...... sion injury in postconditioned

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type

label

Increased mitochondrial calciu ...... ut not preconditioned) hearts.

@en

Increased mitochondrial calciu ...... sion injury in postconditioned

@nl

prefLabel

Increased mitochondrial calciu ...... ut not preconditioned) hearts.

@en

Increased mitochondrial calciu ...... sion injury in postconditioned

@nl

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P356

AJPHEART.01035.2007

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American Journal of Physiology - Heart and Circulatory Physiology

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Increased mitochondrial calciu ...... ut not preconditioned) hearts.

@en

P2093

Dominique Robert

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

Elisabeth Couture-Lepetit

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

Joseph Loufouat

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

Laurent Argaud

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

Lionel Augeul

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

Ludovic Gomez

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

Michel Ovize

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

Odile Gateau-Roesch

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

P2860

Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning

Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death

Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Low-pressure reperfusion alters mitochondrial permeability transition

Mitochondrial targeted cyclophilin D protects cells from cell death by peptidyl prolyl isomerization

Cyclophilin and peptidyl-prolyl cis-trans isomerase are probably identical proteins

Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heart.

Mitochondrial intermembrane junctional complexes and their role in cell death.

Mitochondria as all-round players of the calcium game.

Cyclophilin D, a component of the permeability transition-pore, is an apoptosis repressor.

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10.1152/AJPHEART.01035.2007

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P921

reperfusion injury