CCL2/Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts. - Wikidata - awgldk - TriplyDB

CCL2/Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts.

CCL2/Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts.

http://www.wikidata.org/entity/Q52563229

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Modulation of macrophage activation state protects tissue from necrosis during critical limb ischemia in thrombospondin-1-deficient mice How Biomaterials Can Influence Various Cell Types in the Repair and Regeneration of the Heart after Myocardial Infarction Chemokines and Heart Disease: A Network Connecting Cardiovascular Biology to Immune and Autonomic Nervous Systems Inflammation and Inflammatory Cells in Myocardial Infarction and Reperfusion Injury: A Double-Edged Sword Monocytes in myocardial infarction Communication in the heart: the role of the innate immune system in coordinating cellular responses to ischemic injury Targeting matrix metalloproteinases in heart disease: lessons from endogenous inhibitors Origin of developmental precursors dictates the pathophysiologic role of cardiac fibroblasts Monocyte heterogeneity in cardiovascular disease Anti-Gal: an abundant human natural antibody of multiple pathogeneses and clinical benefits Effector mechanisms of rejection Immune Modulation of Cardiac Repair and Regeneration: The Art of Mending Broken Hearts The Role of CC-Chemokines in the Regulation of Angiogenesis Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries Ischemia and reperfusion related myocardial inflammation: A network of cells and mediators targeting the cardiomyocyte Osteopontin and mucosal protection The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions Oxidative DNA damage caused by inflammation may link to stress-induced non-targeted effects.The role of circulating mesenchymal progenitor cells (fibrocytes) in the pathogenesis of fibrotic disorders.Fibrocytes: bringing new insights into mechanisms of inflammation and fibrosis.Chemokines as mediators of neovascularization Toll-like receptor 4 deficiency: smaller infarcts, but no gain in function.Paracrine factors of mesenchymal stem cells recruit macrophages and endothelial lineage cells and enhance wound healing.Cellular mechanisms of tissue fibrosis. 6. Purinergic signaling and response in fibroblasts and tissue fibrosis Ly-6Chigh monocytes depend on Nr4a1 to balance both inflammatory and reparative phases in the infarcted myocardium.MCP-1 Levels are Associated with Cardiac Remodeling but not with Resistant Hypertension Splenic Ly6Chi monocytes contribute to adverse late post-ischemic left ventricular remodeling in heme oxygenase-1 deficient mice Effects of interleukin-33 on cardiac fibroblast gene expression and activity.Macrophage roles following myocardial infarction CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells Monocytes: protagonists of infarct inflammation and repair after myocardial infarction The role of inflammatory and fibrogenic pathways in heart failure associated with aging.CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans Targeted injection of a biocomposite material alters macrophage and fibroblast phenotype and function following myocardial infarction: relation to left ventricular remodeling Evaluation of Cardiac Function by Transthoracic Echocardiography in Subjects with ST-Segment Elevation Myocardial Infarction Following Primary Percutaneous Coronary Intervention according to Valsartan Dose: The Valsartan One Center Trial.Tumors induce complex DNA damage in distant proliferative tissues in vivo Concise review: bone marrow-derived stem/progenitor cells in cutaneous repair and regeneration.Treatment of diabetic mice with undenatured whey protein accelerates the wound healing process by enhancing the expression of MIP-1α, MIP-2, KC, CX3CL1 and TGF-β in wounded tissue.Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure.Angiotensin-converting enzyme inhibition prevents the release of monocytes from their splenic reservoir in mice with myocardial infarction.

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P2860

CCL2/Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts.

http://www.wikidata.org/entity/Q52563229

description

2005 nî lūn-bûn

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2005年の論文

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年學術文章

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2005年學術文章

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2005年學術文章

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name

CCL2/Monocyte Chemoattractant ...... o healing myocardial infarcts.

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CCL2/Monocyte Chemoattractant ...... o healing myocardial infarcts.

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type

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CCL2/Monocyte Chemoattractant ...... o healing myocardial infarcts.

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CCL2/Monocyte Chemoattractant ...... o healing myocardial infarcts.

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CCL2/Monocyte Chemoattractant ...... o healing myocardial infarcts.

@en

CCL2/Monocyte Chemoattractant ...... o healing myocardial infarcts.

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01.RES.0000163017.13772.3A

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Circulation Research

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CCL2/Monocyte Chemoattractant ...... o healing myocardial infarcts.

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Anna Koerting

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Barrett J Rollins

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Guofeng Ren

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Kim Winkelmann

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Lloyd H Michael

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Mark L Entman

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Nikolaos G Frangogiannis

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Oliver Dewald

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Pawel Zymek

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Tareq Abou-Khamis

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881-889

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scholarly article

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10.1161/01.RES.0000163017.13772.3A

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8

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96

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2005-03-17T00:00:00Z

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