Deletion of macrophage migration inhibitory factor protects the heart from severe ischemia-reperfusion injury: a predominant role of anti-inflammation (Q83152715)

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scientific article published on 06 January 2011

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English	Deletion of macrophage migration inhibitory factor protects the heart from severe ischemia-reperfusion injury: a predominant role of anti-inflammation	scientific article published on 06 January 2011

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19 January 2020

Deletion of macrophage migration inhibitory factor protects the heart from severe ischemia-reperfusion injury: a predominant role of anti-inflammation (English)

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19 January 2020

reperfusion injury

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based on heuristic

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Clinton R. Bruce

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19 January 2020

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19 January 2020

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Xiao-Ming Gao

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19 January 2020

Yang Liu

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19 January 2020

David White

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19 January 2020

Yidan Su

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19 January 2020

Brian G Drew

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19 January 2020

Helen Kiriazis

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19 January 2020

Qi Xu

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19 January 2020

Nicole Jennings

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19 January 2020

Alex Bobik

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19 January 2020

Mark A Febbraio

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19 January 2020

Bronwyn A Kingwell

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19 January 2020

Richard Bucala

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19 January 2020

Günter Fingerle-Rowson

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19 January 2020

Anthony M Dart

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19 January 2020

Xiao-Jun Du

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6 January 2011

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19 January 2020

Journal of Molecular and Cellular Cardiology

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19 January 2020

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19 January 2020

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19 January 2020

991-999

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19 January 2020

The inflammatory response in myocardial infarction

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AMP-activated protein kinase (AMPK) control of fatty acid and glucose metabolism in the ischemic heart

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7 January 2021

The role of neutrophils in myocardial ischemia-reperfusion injury

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Role of apoptosis in reperfusion injury

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Adiponectin-mediated modulation of hypertrophic signals in the heart

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Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms

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Minireview: the AMP-activated protein kinase cascade: the key sensor of cellular energy status.

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AMP-activated protein kinase: a key stress signaling pathway in the heart

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Macrophage migration inhibitory factor in cardiovascular disease

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MIF regulates innate immune responses through modulation of Toll-like receptor 4

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The proinflammatory mediator macrophage migration inhibitory factor induces glucose catabolism in muscle

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Macrophage migration inhibitory factor stimulates AMP-activated protein kinase in the ischaemic heart.

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Impact of a single intravenous administration of nicorandil before reperfusion in patients with ST-segment-elevation myocardial infarction.

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Myocardial ischemia/reperfusion-injury, a clinical view on a complex pathophysiological process

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Expression of active alpha(1B)-adrenergic receptors in the heart does not alleviate ischemic reperfusion injury

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Differences in inflammation, MMP activation and collagen damage account for gender difference in murine cardiac rupture following myocardial infarction

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AMP-activated protein kinase phosphorylation of endothelial NO synthase

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Toll-like receptor signaling in the ischemic heart

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Expression of Macrophage Migration Inhibitory Factor in Acute Ischemic Myocardial Injury

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Elevation of plasma level of macrophage migration inhibitory factor in patients with acute myocardial infarction

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Increase of macrophage migration inhibitory factor (MIF) expression in cardiomyocytes during chronic hypoxia.

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The role of macrophage migration inhibitory factor in the cascade of events leading to reperfusion-induced inflammatory injury and lethality

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Macrophage migration inhibitory factor (MIF) sustains macrophage proinflammatory function by inhibiting p53: regulatory role in the innate immune response

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Of mice and dogs: species-specific differences in the inflammatory response following myocardial infarction.

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Elevated plasma levels of interleukin-1 receptor antagonist and interleukin-10 in patients with acute myocardial infarction

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Interplay of TNF-alpha and IL-10 in regulating oxidative stress in isolated adult cardiac myocytes

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Endotoxin-induced myocardial dysfunction: effects of macrophage migration inhibitory factor neutralization

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Blockade of macrophage migration inhibitory factor ameliorates experimental autoimmune myocarditis

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10.1016/J.YJMCC.2010.12.022

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19 January 2020

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19 January 2020

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