Inhibition of GSK3beta by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion.
about
Inhibition of the Mitochondrial Permeability Transition for Cytoprotection: Direct versus Indirect MechanismsRole of the MPTP in conditioning the heart - translatability and mechanismThe GSK-3 family as therapeutic target for myocardial diseasesMyocardial autophagic energy stress responses--macroautophagy, mitophagy, and glycophagyPostconditioning signalling in the heart: mechanisms and translatabilityCytoprotection by the modulation of mitochondrial electron transport chain: the emerging role of mitochondrial STAT3Intermittent losartan administration triggers cardiac post-conditioning in isolated rat hearts: role of BK2 receptorsA New Therapeutic Modality for Acute Myocardial Infarction: Nanoparticle-Mediated Delivery of Pitavastatin Induces Cardioprotection from Ischemia-Reperfusion Injury via Activation of PI3K/Akt Pathway and Anti-Inflammation in a Rat ModelSelective blockade of protein kinase B protects the rat and human myocardium against ischaemic injuryAkt: A Therapeutic Target in Hepatic Ischemia-Reperfusion Injury.Volatile anesthetic post-treatment induces protection via inhibition of glycogen synthase kinase 3β in human neuron-like cells.Involvment of cytosolic and mitochondrial GSK-3beta in mitochondrial dysfunction and neuronal cell death of MPTP/MPP-treated neuronsA novel estrogen receptor GPER inhibits mitochondria permeability transition pore opening and protects the heart against ischemia-reperfusion injury.Cardioprotection leads to novel changes in the mitochondrial proteome.Protein Kinase Signaling at the Crossroads of Myocyte Life and Death in Ischemic Heart Disease.Pharmacological postconditioning with atorvastatin calcium attenuates myocardial ischemia/reperfusion injury in diabetic rats by phosphorylating GSK3β.Mitochondrial kinase signalling pathways in myocardial protection from ischaemia/reperfusion-induced necrosis.Blockade of electron transport during ischemia preserves bcl-2 and inhibits opening of the mitochondrial permeability transition poreHydrogen sulfide preconditioning protects rat liver against ischemia/reperfusion injury by activating Akt-GSK-3β signaling and inhibiting mitochondrial permeability transition.MG53 participates in ischaemic postconditioning through the RISK signalling pathwayInhibition of glycogen synthase kinase 3 beta ameliorates liver ischemia reperfusion injury by way of an interleukin-10-mediated immune regulatory mechanism.Pharmacological postconditioning effect of muramyl dipeptide is mediated through RIP2 and TAK1Morphine-induced postconditioning modulates mitochondrial permeability transition pore opening via delta-1 opioid receptors activation in isolated rat hearts.Intracellular zinc release-activated ERK-dependent GSK-3β-p53 and Noxa-Mcl-1 signaling are both involved in cardiac ischemic-reperfusion injury.How the Wnt signaling pathway protects from neurodegeneration: the mitochondrial scenarioTransgenic over expression of ectonucleotide triphosphate diphosphohydrolase-1 protects against murine myocardial ischemic injury.Cardioprotection by H2S engages a cGMP-dependent protein kinase G/phospholamban pathway.RETRACTED: Glycogen synthase kinase 3β transfers cytoprotective signaling through connexin 43 onto mitochondrial ATP-sensitive K+ channels.G Protein-Coupled Estrogen Receptor 1 Mediates Acute Estrogen-Induced Cardioprotection via MEK/ERK/GSK-3β Pathway after Ischemia/Reperfusion.Phosphorylation of GSK-3β mediates intralipid-induced cardioprotection against ischemia/reperfusion injury.Remote Ischemic Postconditioning Ameliorates the Mesenchymal Stem Cells Engraftment in Reperfused Myocardium.Endogenous cardioprotection by ischaemic postconditioning and remote conditioning.Blockade of electron transport at the onset of reperfusion decreases cardiac injury in aged hearts by protecting the inner mitochondrial membrane.The Dose-Dependent Organ-Specific Effects of a Dipeptidyl Peptidase-4 Inhibitor on Cardiovascular Complications in a Model of Type 2 DiabetesA novel role for mitochondrial sphingosine-1-phosphate produced by sphingosine kinase-2 in PTP-mediated cell survival during cardioprotection.Acute inhibition of GSK causes mitochondrial remodeling.Cyclosporin variably and inconsistently reduces infarct size in experimental models of reperfused myocardial infarction: a systematic review and meta-analysis.Aldose reductase modulates cardiac glycogen synthase kinase-3β phosphorylation during ischemia-reperfusion.Involvement of Glycogen Synthase Kinase-3β and Oxidation Status in the Loss of Cardioprotection by Postconditioning in Chronic Diabetic Male Rats.Astragaloside IV inhibits oxidative stress-induced mitochondrial permeability transition pore opening by inactivating GSK-3β via nitric oxide in H9c2 cardiac cells.
P2860
Q21296696-F83817AF-0528-4D57-B092-2BA06A481D2DQ26830560-699B64CA-3388-406A-A403-551E6ABB752BQ26861134-C144F8A8-4942-4487-8B07-B5C248D3ECD4Q26995370-C6D685E8-E00F-4A89-8189-8DE02911FFFAQ27021021-2E03651D-C356-465D-962E-81C75CDC8970Q28396645-C602F987-7565-4CFE-A1F5-89C7A092D58FQ28539671-0F3998FC-5273-472B-B906-9EDC7415434EQ28546468-37DCB88C-0EA1-4E1C-8AE0-E3E00E0C7EA4Q28567327-829E5CEA-C01B-4EC3-A10F-8998EEEFD230Q30248771-F0756732-4DB1-453C-BB98-2D6B329B3E45Q30427390-47B080F5-C68E-4B5E-A239-4D8A5EE7C596Q33442821-6ED59356-E60D-4ADD-8B91-DCA901645043Q33589179-997D9F3E-B1EB-43EC-944A-494D15414967Q33589244-1029CD31-39CA-4D99-80C0-4BAB8C8FC4A3Q33604010-6C79D69E-CDE1-423D-94C0-46ABAAB3A206Q33846404-0731EA47-9193-4D2C-8CBC-0BFF61600DCDQ34620765-B1C091F9-03E9-4349-9A37-A547E87086E5Q34792021-A1358358-EBD6-427C-8936-4EC6D37C319FQ34994670-29590852-0389-4C69-9875-1ABF7D3CE927Q35037331-5AA18A58-8202-4FAE-8728-CA3DF7C29E68Q35131974-B09BB4B4-C7A1-4286-AD3F-63C17CFFC93EQ35135046-9BB6F90F-BB96-4D0B-811B-127015C8E6ABQ35161515-ECCB883C-8AD3-4E9B-9BBA-A55B8002F665Q35210645-63CD35A6-59EE-4AAF-8661-18F2DF9E58A1Q35569964-4A14B183-318B-4209-9135-3B3117015565Q35632965-FF4D6647-9837-45F6-BE69-9EC143464519Q35661834-07831611-5BB6-4C6D-AEBF-6E555A6843ABQ35749776-59AB05CE-698C-44C4-8F68-FD51C9D96696Q35769417-9D7A9B40-C257-4432-B933-CE94F48A5EC1Q35877872-2A3C0DB3-CEC0-4CA3-BD66-ED1F4871295DQ35892642-2FB47C7C-9928-4586-8A35-36F0835A5286Q35902467-A0C4C95E-31FC-49AB-A34C-7D683899A515Q35944872-23ED97FF-C500-4F12-92FE-AF1A10039F92Q35951020-D5F10456-308C-4112-A2F6-5F4F257A7C90Q36011190-F51F6139-C40B-4CB4-ACC0-911BFD7DD0F1Q36042607-8491A25A-6C09-4DF5-9DE8-E79E609120C0Q36147255-3A50B923-196E-486C-B859-3C04AC99A2D3Q36176141-0C611AE3-C299-41F7-A8A5-F69E7BC2497AQ36196031-F0985A1D-A4D2-4E7C-ADE7-889A0AD6C4A2Q36294287-7A238100-9FCA-404B-90EC-CCD6C525A58E
P2860
Inhibition of GSK3beta by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh-hant
name
Inhibition of GSK3beta by post ...... ition pore during reperfusion.
@en
Inhibition of GSK3beta by post ...... ition pore during reperfusion.
@nl
type
label
Inhibition of GSK3beta by post ...... ition pore during reperfusion.
@en
Inhibition of GSK3beta by post ...... ition pore during reperfusion.
@nl
prefLabel
Inhibition of GSK3beta by post ...... ition pore during reperfusion.
@en
Inhibition of GSK3beta by post ...... ition pore during reperfusion.
@nl
P2093
P1433
P1476
Inhibition of GSK3beta by post ...... ition pore during reperfusion.
@en
P2093
Hélène Thibault
Ludovic Gomez
Michel Ovize
P304
P356
10.1161/CIRCULATIONAHA.107.755066
P407
P577
2008-05-19T00:00:00Z