Inhibition of c-Jun-N-terminal kinase increases cardiac peroxisome proliferator-activated receptor alpha expression and fatty acid oxidation and prevents lipopolysaccharide-induced heart dysfunction.
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PPARs: Protectors or Opponents of Myocardial Function?Metformin protects against infection-induced myocardial dysfunction.Periostin promotes liver steatosis and hypertriglyceridemia through downregulation of PPARα.PPARγ signaling is required for mediating EETs protective effects in neonatal cardiomyocytes exposed to LPSA broad activity screen in support of a chemogenomic map for kinase signalling research and drug discovery.Targeting extracellular DNA to deliver IGF-1 to the injured heartPathophysiology of sepsis-related cardiac dysfunction: driven by inflammation, energy mismanagement, or both?Case report: severe reversible cardiomyopathy associated with systemic inflammatory response syndrome in the setting of diabetic hyperosmolar hyperglycemic non-ketotic syndrome.A Double-Blind, Placebo-Controlled Trial to Evaluate the Safety, Tolerability, and Pharmacokinetics of Single, Escalating Oral Doses of JDTic.Cardiac lipotoxicity: molecular pathways and therapeutic implications.Enhanced Glucose Transport, but not Phosphorylation Capacity, Ameliorates Lipopolysaccharide-Induced Impairments in Insulin-Stimulated Muscle Glucose Uptake.Peroxisome proliferator-activated receptor-γ activation prevents sepsis-related cardiac dysfunction and mortality in mice.Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac FunctionThe involvement of regulatory non-coding RNAs in sepsis: a systematic review.Lipid Use and Misuse by the Heart.Treatment of endotoxaemia and septicaemia in the equine patient.PPARα augments heart function and cardiac fatty acid oxidation in early experimental polymicrobial sepsis.Nonhematopoietic Peroxisome Proliferator-Activated Receptor-α Protects Against Cardiac Injury and Enhances Survival in Experimental Polymicrobial Sepsis.PPAR-γ Activation Prevents Septic Cardiac Dysfunction via Inhibition of Apoptosis and NecroptosisInhibition of NADPH oxidase 2 (NOX2) prevents sepsis-induced cardiomyopathy by improving calcium handling and mitochondrial function.The Relationship Between KLF5 and PPARα in the Heart: It's Complicated.Early antagonism of cerebral high mobility group box-1 protein is benefit for sepsis induced brain injury.Mitochondrial-Targeted Antioxidant MitoQ Prevents Lipopolysaccharide-Induced Accumulation of Triacylglycerol and Lipid Droplets Biogenesis in Epithelial Cells
P2860
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P2860
Inhibition of c-Jun-N-terminal kinase increases cardiac peroxisome proliferator-activated receptor alpha expression and fatty acid oxidation and prevents lipopolysaccharide-induced heart dysfunction.
description
2011 nî lūn-bûn
@nan
2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Inhibition of c-Jun-N-terminal ...... ide-induced heart dysfunction.
@ast
Inhibition of c-Jun-N-terminal ...... ide-induced heart dysfunction.
@en
type
label
Inhibition of c-Jun-N-terminal ...... ide-induced heart dysfunction.
@ast
Inhibition of c-Jun-N-terminal ...... ide-induced heart dysfunction.
@en
prefLabel
Inhibition of c-Jun-N-terminal ...... ide-induced heart dysfunction.
@ast
Inhibition of c-Jun-N-terminal ...... ide-induced heart dysfunction.
@en
P2093
P2860
P356
P1476
Inhibition of c-Jun-N-terminal ...... ride-induced heart dysfunction
@en
P2093
Ira J Goldberg
P Christian Schulze
Raffay Khan
Shunichi Homma
Zoi Drosatos-Tampakaki
P2860
P304
36331-36339
P356
10.1074/JBC.M111.272146
P407
P577
2011-08-26T00:00:00Z