Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing. - Wikidata - awgldk - TriplyDB

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

http://www.wikidata.org/entity/Q37974118

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How Biomaterials Can Influence Various Cell Types in the Repair and Regeneration of the Heart after Myocardial Infarction Ischemia and reperfusion related myocardial inflammation: A network of cells and mediators targeting the cardiomyocyte Cyclovirobuxinum D suppresses lipopolysaccharide-induced inflammatory responses in murine macrophages in vitro by blocking JAK-STAT signaling pathway.Modulation of mononuclear phagocyte inflammatory response by liposome-encapsulated voltage gated sodium channel inhibitor ameliorates myocardial ischemia/reperfusion injury in rats.Deficiency of ataxia telangiectasia mutated kinase modulates cardiac remodeling following myocardial infarction: involvement in fibrosis and apoptosis.Dexmedetomidine preconditioning may attenuate myocardial ischemia/reperfusion injury by down-regulating the HMGB1-TLR4-MyD88-NF-кB signaling pathway Matrix metalloproteinases: drug targets for myocardial infarction.Image-guided therapies for myocardial repair: concepts and practical implementation.Mechanisms and consequences of inflammatory signaling in the myocardium.Macrophages' Role in Tissue Disease and Regeneration.Stanniocalcin-1 attenuates ischemic cardiac injury and response of differentiating monocytes/macrophages to inflammatory stimuli Monocytes increase human cardiac myofibroblast-mediated extracellular matrix remodeling through TGF-β1.Targeting Amino Acid Metabolism for Molecular Imaging of Inflammation Early After Myocardial Infarction.Knockdown of TNF-α by DNAzyme gold nanoparticles as an anti-inflammatory therapy for myocardial infarction Myoblast transplantation improves cardiac function after myocardial infarction through attenuating inflammatory responses.Dual-targeting Theranostic System with Mimicking Apoptosis to Promote Myocardial Infarction Repair via Modulation of Macrophages.Rev-erb agonist improves adverse cardiac remodeling and survival in myocardial infarction through an anti-inflammatory mechanism.Targeting post-infarct inflammation by PET imaging: comparison of (68)Ga-citrate and (68)Ga-DOTATATE with (18)F-FDG in a mouse model.Pretreatment with fish oil attenuates heart ischaemia consequences in rats.Pharmacological inhibition of the triggering receptor expressed on myeloid cells-1 limits reperfusion injury in a porcine model of myocardial infarction.Current Trends in Biomaterial Utilization for Cardiopulmonary System Regeneration.

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P2860

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

http://www.wikidata.org/entity/Q37974118

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article científic

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article scientifique

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articol științific

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articolo scientifico

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artigo científico

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artigo científico

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artigo científico

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artikel ilmiah

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artikull shkencor

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artículo científico

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name

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

@en

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

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type

label

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

@en

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

@nl

prefLabel

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

@en

Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

@nl

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S00109-011-0847-Y

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Journal of Molecular Medicine

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Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

@en

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Kai C Wollert

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

Tibor Kempf

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P2860

The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions

Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6

The role of endothelial PI3Kgamma activity in neutrophil trafficking.

The transforming growth factor-beta superfamily member growth-differentiation factor-15 protects the heart from ischemia/reperfusion injury.

CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells

Myocardial knockdown of mRNA-stabilizing protein HuR attenuates post-MI inflammatory response and left ventricular dysfunction in IL-10-null mice.

CXCR4 blockade augments bone marrow progenitor cell recruitment to the neovasculature and reduces mortality after myocardial infarction

Monocytes: protagonists of infarct inflammation and repair after myocardial infarction

Angiotensin-converting enzyme inhibition prevents the release of monocytes from their splenic reservoir in mice with myocardial infarction.

Modulation of cardiac macrophages by phosphatidylserine-presenting liposomes improves infarct repair.

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s00109-011-0847-y

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361-369

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scholarly article

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10.1007/S00109-011-0847-Y

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4

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90

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Alexander Zarbock

Dietmar Vestweber

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2012-01-07T00:00:00Z

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22228177

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