High-mobility group box-1 protein promotes angiogenesis after peripheral ischemia in diabetic mice through a VEGF-dependent mechanism. - Wikidata - awgldk - TriplyDB

High-mobility group box-1 protein promotes angiogenesis after peripheral ischemia in diabetic mice through a VEGF-dependent mechanism.

High-mobility group box-1 protein promotes angiogenesis after peripheral ischemia in diabetic mice through a VEGF-dependent mechanism.

http://www.wikidata.org/entity/Q33869816

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Disruption of a Regulatory Network Consisting of Neutrophils and Platelets Fosters Persisting Inflammation in Rheumatic Diseases Innate Immunity and Inflammation Post-Stroke: An α7-Nicotinic Agonist Perspective High-mobility group box 1: an amplifier of stem and progenitor cell activity after stroke Vitreous mediators in retinal hypoxic diseases Skeletal myofiber VEGF is essential for the exercise training response in adult mice Glycaemic variability affects ischaemia-induced angiogenesis in diabetic mice.Toward a mouse model of hind limb ischemia to test therapeutic angiogenesis HMGB1 and TLR4 mediate skeletal muscle recovery in a murine model of hindlimb ischemia.HMGB1 in health and disease.TLR4 accessory molecule RP105 (CD180) regulates monocyte-driven arteriogenesis in a murine hind limb ischemia model.The high-mobility group box-1 nuclear factor mediates retinal injury after ischemia reperfusion.Diabetes: impaired damage control HMGB1 contributes to allergen-induced airway remodeling in a murine model of chronic asthma by modulating airway inflammation and activating lung fibroblasts High-mobility group box 1 protein is implicated in advanced glycation end products-induced vascular endothelial growth factor A production in the rat retinal ganglion cell line RGC-5.Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) enhances engraftment and angiogenesis of mesenchymal stem cells in diabetic hindlimb ischemia.TLR4 Deters Perfusion Recovery and Upregulates Toll-like Receptor 2 (TLR2) in Ischemic Skeletal Muscle and Endothelial Cells HMGB1 in renal ischemic injury.The alarmin HMGB-1 influences healing outcomes in fetal skin wounds High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury.HMGB1 Promotes Intraoral Palatal Wound Healing through RAGE-Dependent Mechanisms.Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke.Cardiovascular disease and high-mobility group box 1--is a new inflammatory killer in town?High-mobility group box 1 protein activating nuclear factor-κB to upregulate vascular endothelial growth factor C is involved in lymphangiogenesis and lymphatic node metastasis in colon cancer.Cellular mechanisms of high mobility group 1 (HMGB-1) protein action in the diabetic retinopathy.Redox status of high-mobility group box 1 performs a dual role in angiogenesis of colorectal carcinoma.Prognostic value of the high-mobility group box-1 in young patients with chest pain.High-mobility group box 1 inhibits gastric ulcer healing through Toll-like receptor 4 and receptor for advanced glycation end products.Soluble receptor for advanced glycation end products alleviates nephritis in (NZB/NZW)F1 mice.Tumor angiogenesis is enforced by autocrine regulation of high-mobility group box 1.The Role of High-Mobility Group Box-1 and Its Crosstalk with Microbiome in Rheumatoid Arthritis.Basic Fibroblast Growth Factor Protects Astrocytes Against Ischemia/Reperfusion Injury by Upregulating the Caveolin-1/VEGF Signaling Pathway.HMGB1-induced angiogenesis in perforated disc cells of human temporomandibular joint.Markers of endothelial dysfunction in patients with non-alcoholic fatty liver disease and coronary artery disease.The role of high-mobility group box protein 1 in collagen antibody-induced arthritis is dependent on vascular endothelial growth factor.Suppression of Receptor for Advanced Glycation End Products Improves Angiogenic Responses to Ischemia in Diabetic Mouse Hindlimb Ischemia Model

P2860

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P2860

High-mobility group box-1 protein promotes angiogenesis after peripheral ischemia in diabetic mice through a VEGF-dependent mechanism.

http://www.wikidata.org/entity/Q33869816

description

2010 nî lūn-bûn

@nan

2010 թուականի Մարտին հրատարակուած գիտական յօդուած

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2010 թվականի մարտին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

@yue

2010年論文

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2010年論文

@zh-hk

2010年論文

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2010年論文

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2010年论文

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name

High-mobility group box-1 prot ...... gh a VEGF-dependent mechanism.

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High-mobility group box-1 prot ...... gh a VEGF-dependent mechanism.

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type

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High-mobility group box-1 prot ...... gh a VEGF-dependent mechanism.

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High-mobility group box-1 prot ...... gh a VEGF-dependent mechanism.

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prefLabel

High-mobility group box-1 prot ...... gh a VEGF-dependent mechanism.

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High-mobility group box-1 prot ...... gh a VEGF-dependent mechanism.

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High-mobility group box-1 prot ...... ugh a VEGF-dependent mechanism

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P2093

Andrea Flex

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

Egidio Stigliano

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

Giovanni Ghirlanda

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

Giovanni Pecorini

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

Giuseppe Straface

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

Kensuke Egashira

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

Paola Rizzo

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

Stefano Lancellotti

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

Vincenzo Arena

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

P2860

Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation

Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

HMG-1 as a late mediator of endotoxin lethality in mice

Cutting edge: extracellular high mobility group box-1 protein is a proangiogenic cytokine

The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of rage and amphoterin in the developing nervous system

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

High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes

Amphoterin stimulates myogenesis and counteracts the antimyogenic factors basic fibroblast growth factor and S100B via RAGE binding

Rescue of diabetes-related impairment of angiogenesis by intramuscular gene therapy with adeno-VEGF.

Mouse model of angiogenesis

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1496-1505

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scholarly article

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10.2337/DB09-1507

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6

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59

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Raimondo De Cristofaro

Federico Biscetti

Giulia De Angelis

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2010-03-03T00:00:00Z

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41722125

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20200317

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2874711

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