HMGB1-Driven Inflammation and Intimal Hyperplasia After Arterial Injury Involves Cell-Specific Actions Mediated by TLR4. - Wikidata - wikimedia - TriplyDB

HMGB1-Driven Inflammation and Intimal Hyperplasia After Arterial Injury Involves Cell-Specific Actions Mediated by TLR4.

HMGB1-Driven Inflammation and Intimal Hyperplasia After Arterial Injury Involves Cell-Specific Actions Mediated by TLR4.

http://www.wikidata.org/entity/Q36935091

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Anti-high mobility group box-1 (HMGB1) antibody attenuates delayed cerebral vasospasm and brain injury after subarachnoid hemorrhage in rats Cathepsin L promotes Vascular Intimal Hyperplasia after Arterial Injury High Mobility Group Box-1 Promotes Inflammation-Induced Lymphangiogenesis via Toll-Like Receptor 4-Dependent Signalling Pathway.Calcineurin inhibitors cyclosporine A and tacrolimus induce vascular inflammation and endothelial activation through TLR4 signaling.Infiltration of M1, but not M2, macrophages is impaired after unilateral ureter obstruction in Nrf2-deficient mice.Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression.Pulmonary Epithelial TLR4 Activation Leads to Lung Injury in Neonatal Necrotizing Enterocolitis.Identification of specifically activated angiogenic molecules in HMGB-1-induced angiogenesis.BLTR1 in Monocytes Emerges as a Therapeutic Target For Vascular Inflammation With a Subsequent Intimal Hyperplasia in a Murine Wire-Injured Femoral Artery

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HMGB1-Driven Inflammation and Intimal Hyperplasia After Arterial Injury Involves Cell-Specific Actions Mediated by TLR4.

http://www.wikidata.org/entity/Q36935091

description

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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HMGB1-Driven Inflammation and ...... ific Actions Mediated by TLR4.

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HMGB1-Driven Inflammation and ...... ific Actions Mediated by TLR4.

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HMGB1-Driven Inflammation and ...... ific Actions Mediated by TLR4.

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Arteriosclerosis, Thrombosis, and Vascular Biology

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HMGB1-Driven Inflammation and ...... ific Actions Mediated by TLR4.

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P2093

Alex F Chen

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

Ben Lu

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

Dandan Chen

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

David J Hackam

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

Hong Yuan

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

Huan Yang

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

Jiemei Wang

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

Jingjing Cai

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

Jinze Wu

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

John P Pribis

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

P2860

Intravascular brachytherapy for peripheral vascular disease

Signal transduction by the lipopolysaccharide receptor, Toll-like receptor-4

The lack of chromosomal protein Hmg1 does not disrupt cell growth but causes lethal hypoglycaemia in newborn mice

HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses

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

Toll-like receptors: critical proteins linking innate and acquired immunity

The many faces of HMGB1: molecular structure-functional activity in inflammation, apoptosis, and chemotaxis.

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

Inflammation and restenosis in the stent era.

Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1)

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2579-2593

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scholarly article

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10.1161/ATVBAHA.115.305789

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12

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35

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Kevin J. Tracey

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2015-10-29T00:00:00Z

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26515416

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Toll-like receptor

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4880018

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