Expression of high-mobility group box 1 and of receptor for advanced glycation end products in chronic obstructive pulmonary disease. - Wikidata - wikimedia - TriplyDB

Expression of high-mobility group box 1 and of receptor for advanced glycation end products in chronic obstructive pulmonary disease.

Expression of high-mobility group box 1 and of receptor for advanced glycation end products in chronic obstructive pulmonary disease.

http://www.wikidata.org/entity/Q39743331

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The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation Association between HMGB1 and COPD: A Systematic Review RAGE: a new frontier in chronic airways disease Systemic biomarkers of neutrophilic inflammation, tissue injury and repair in COPD patients with differing levels of disease severity Diesel particulate matter induces receptor for advanced glycation end-products (RAGE) expression in pulmonary epithelial cells, and RAGE signaling influences NF-κB-mediated inflammation Individual and cumulative effects of GWAS susceptibility loci in lung cancer: associations after sub-phenotyping for COPD Cytokine inhibition in the treatment of COPD.Soluble receptor for advanced glycation end-products and progression of airway disease Smoking exposure induces human lung endothelial cell adaptation to apoptotic stress.2-O, 3-O-desulfated heparin inhibits neutrophil elastase-induced HMGB-1 secretion and airway inflammation.Changes of HMGB1 and sRAGE during the recovery of COPD exacerbation Receptor for advanced glycation endproducts (RAGE) maintains pulmonary structure and regulates the response to cigarette smoke.Sputum biomarkers and the prediction of clinical outcomes in patients with cystic fibrosis.Innate immunity but not NLRP3 inflammasome activation correlates with severity of stable COPD.HMGB1 in health and disease.Targeting pro-resolution pathways to combat chronic inflammation in COPD Soluble receptor for advanced glycation end products in COPD: relationship with emphysema and chronic cor pulmonale: a case-control study.Update in chronic obstructive pulmonary disease in 2010.High mobility group box 1 induced human lung myofibroblasts differentiation and enhanced migration by activation of MMP-9.High mobility group protein B1 (HMGB1) in Asthma: comparison of patients with chronic obstructive pulmonary disease and healthy controls.Role of interleukin-1 and MyD88-dependent signaling in rhinovirus infection.High-mobility group box-1 induces vascular remodelling processes via c-Jun activation HMGB1 contributes to allergen-induced airway remodeling in a murine model of chronic asthma by modulating airway inflammation and activating lung fibroblasts Stress responses affecting homeostasis of the alveolar capillary unit.Cadmium-mediated toxicity of lung epithelia is enhanced through NF-κB-mediated transcriptional activation of the human zinc transporter ZIP8.Therapeutic effects of LASSBio-596 in an elastase-induced mouse model of emphysema Pathogenesis of chronic obstructive pulmonary disease The Ser82 RAGE Variant Affects Lung Function and Serum RAGE in Smokers and sRAGE Production In Vitro.High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells.High-mobility group box 1 impairs airway epithelial barrier function through the activation of the RAGE/ERK pathway.Advanced glycation endproducts and their receptor in different body compartments in COPD Inflammation and immune response in COPD: where do we stand?New insights into mechanisms controlling the NLRP3 inflammasome and its role in lung disease.Association of plasma sRAGE, but not esRAGE with lung function impairment in COPD.Association of polymorphisms of the receptor for advanced glycation end products gene with COPD in the Chinese population.Functional interactors of three genome-wide association study genes are differentially expressed in severe chronic obstructive pulmonary disease lung tissue.Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases Lung damage and airway remodelling in severe asthma.Phenotyping the heterogeneity of chronic obstructive pulmonary disease.DAMPs activating innate and adaptive immune responses in COPD.

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Expression of high-mobility group box 1 and of receptor for advanced glycation end products in chronic obstructive pulmonary disease.

http://www.wikidata.org/entity/Q39743331

description

2010 nî lūn-bûn

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2010年の論文

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年學術文章

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2010年學術文章

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2010年學術文章

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name

Expression of high-mobility gr ...... obstructive pulmonary disease.

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Expression of high-mobility gr ...... obstructive pulmonary disease.

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type

label

Expression of high-mobility gr ...... obstructive pulmonary disease.

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Expression of high-mobility gr ...... obstructive pulmonary disease.

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Expression of high-mobility gr ...... obstructive pulmonary disease.

@en

Expression of high-mobility gr ...... obstructive pulmonary disease.

@nl

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RCCM.200903-0340OC

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American Journal of Respiratory and Critical Care Medicine

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Expression of high-mobility gr ...... obstructive pulmonary disease.

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P2093

Alexander Kozhich

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

Anthony J Coyle

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Gary P Sims

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Marie-Christine Dombret

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Marielle Maret

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Marina Pretolani

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Martine Grandsaigne

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Michel Aubier

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Nassima Ferhani

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Olivier Thibaudeau

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P2860

Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease

The nuclear protein HMGB1 is secreted by monocytes via a non-classical, vesicle-mediated secretory pathway

The balance between IL-1 and IL-1Ra in disease

HMGB1 loves company

Receptor for advanced glycation end-products is a marker of type I cell injury in acute lung injury

The high mobility group (HMG) boxes of the nuclear protein HMG1 induce chemotaxis and cytoskeleton reorganization in rat smooth muscle cells

Extracellular HMGB1, a signal of tissue damage, induces mesoangioblast migration and proliferation

Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE

Advanced glycation end products induce tubular epithelial-myofibroblast transition through the RAGE-ERK1/2 MAP kinase signaling pathway

Altered Nrf2/Keap1-Bach1 equilibrium in pulmonary emphysema.

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917-927

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scholarly article

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10.1164/RCCM.200903-0340OC

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9

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181

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2010-02-04T00:00:00Z

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20133931

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chronic obstructive pulmonary disease