When are pro-inflammatory cytokines SAFE in heart failure?
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From basic mechanisms to clinical applications in heart protection, new players in cardiovascular diseases and cardiac theranostics: meeting report from the third international symposium on "New frontiers in cardiovascular research"Heme oxygenase-1 prevents cardiac dysfunction in streptozotocin-diabetic mice by reducing inflammation, oxidative stress, apoptosis and enhancing autophagyQishenyiqi protects ligation-induced left ventricular remodeling by attenuating inflammation and fibrosis via STAT3 and NF-κB signaling pathwayDiacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarctionUpdate on the Pathophysiological Role of Intracellular Signaling Pathways in Atherosclerotic Plaques and Ischemic MyocardiumJAK/STAT3 pathway inhibition blocks skeletal muscle wasting downstream of IL-6 and in experimental cancer cachexia.Pressure overload-induced cardiac remodeling and dysfunction in the absence of interleukin 6 in miceInflammation, adiposity, and mortality in the oldest old.Interleukin 6-preconditioned neural stem cells reduce ischaemic injury in stroke mice.Adipose stromal cells primed with hypoxia and inflammation enhance cardiomyocyte proliferation rate in vitro through STAT3 and Erk1/2.Deletion of Fn14 receptor protects from right heart fibrosis and dysfunctionImpaired exercise capacity and skeletal muscle function in a mouse model of pulmonary inflammation.Differential STAT3 signaling in the heart: Impact of concurrent signals and oxidative stress.High density lipoprotein/sphingosine-1-phosphate-induced cardioprotection: Role of STAT3 as part of the SAFE pathway.Adaptive inflammatory microenvironment for cell-based regeneration in ischemic cardiovascular disease.Neuronal over-expression of ACE2 protects brain from ischemia-induced damageInflammatory cytokines in heart failure: mediators and markers.TWEAK-Fn14 Cytokine-Receptor Axis: A New Player of Myocardial Remodeling and Cardiac FailureUnderstanding STAT3 signaling in cardiac ischemia.Activation of mitochondrial STAT-3 and reduced mitochondria damage during hypothermia treatment for post-cardiac arrest myocardial dysfunction.TNFR2 Stimulation Promotes Mitochondrial Fusion via Stat3- and NF-kB-Dependent Activation of OPA1 Expression.Cardiomyocyte mitochondria as targets of humoral factors released by remote ischemic preconditioning.The SAFE pathway for cardioprotection: is this a promising target?Genetic deletion of the adaptor protein p66Shc increases susceptibility to short-term ischaemic myocardial injury via intracellular salvage pathways.
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When are pro-inflammatory cytokines SAFE in heart failure?
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 07 February 2011
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
When are pro-inflammatory cytokines SAFE in heart failure?
@en
When are pro-inflammatory cytokines SAFE in heart failure?
@nl
type
label
When are pro-inflammatory cytokines SAFE in heart failure?
@en
When are pro-inflammatory cytokines SAFE in heart failure?
@nl
prefLabel
When are pro-inflammatory cytokines SAFE in heart failure?
@en
When are pro-inflammatory cytokines SAFE in heart failure?
@nl
P2860
P356
P1476
When are pro-inflammatory cytokines SAFE in heart failure?
@en
P2093
Richard W James
Sandrine Lecour
P2860
P304
P356
10.1093/EURHEARTJ/EHQ484
P577
2011-02-07T00:00:00Z