RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine model. - Wikidata - wikimedia - TriplyDB

RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine model.

RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine model.

http://www.wikidata.org/entity/Q46775210

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Soluble Receptor for Advanced Glycation End Product: A Biomarker for Acute Coronary Syndrome Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.The spleen contributes importantly to myocardial infarct exacerbation during post-ischemic reperfusion in mice via signaling between cardiac HMGB1 and splenic RAGE.RAGE modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK-3beta signaling pathways.The RAGE axis: a fundamental mechanism signaling danger to the vulnerable vasculature Advanced glycation end product (AGE)-receptor for AGE (RAGE) signaling and up-regulation of Egr-1 in hypoxic macrophages Soluble RAGE: therapy and biomarker in unraveling the RAGE axis in chronic disease and aging Cardiomyocyte aldose reductase causes heart failure and impairs recovery from ischemia.Acute administration of n-3 rich triglyceride emulsions provides cardioprotection in murine models after ischemia-reperfusion Small Molecule Inhibition of Ligand-Stimulated RAGE-DIAPH1 Signal Transduction S100B protein expression in the heart of deceased individuals by overdose: a new forensic marker?A soluble receptor for advanced glycation end-products inhibits hypoxia/reoxygenation-induced apoptosis in rat cardiomyocytes via the mitochondrial pathway.Interaction of β1-adrenoceptor with RAGE mediates cardiomyopathy via CaMKII signaling.RAGE and modulation of ischemic injury in the diabetic myocardium Imaging of receptors for advanced glycation end products in experimental myocardial ischemia and reperfusion injury sRAGE induces human monocyte survival and differentiation Inhibition of Janus activated kinase-3 protects against myocardial ischemia and reperfusion injury in mice.Advanced oxidation protein products induce cardiomyocyte death via Nox2/Rac1/superoxide-dependent TRAF3IP2/JNK signaling.Radical roles for RAGE in the pathogenesis of oxidative stress in cardiovascular diseases and beyond.Receptor for advanced glycation end-products (RAGE) and soluble RAGE (sRAGE): cardiovascular implications.Effect of chronic hypoxia on RAGE and its soluble forms in lungs and plasma of mice.The receptor for advanced glycation endproducts (RAGE) and cardiovascular disease.Tempering the wrath of RAGE: an emerging therapeutic strategy against diabetic complications, neurodegeneration, and inflammation Participation of the receptor for advanced glycation end products in efferocytosis.Sevoflurane postconditioning protects the myocardium against ischemia/reperfusion injury via activation of the JAK2-STAT3 pathway.Advanced glycation endproducts: from precursors to RAGE: round and round we go.Biomarkers in acute lung injury: insights into the pathogenesis of acute lung injury.The potential effects of anti-diabetic medications on myocardial ischemia-reperfusion injury.Cell signaling and receptors in toxicity of advanced glycation end products (AGEs): α-dicarbonyls, radicals, oxidative stress and antioxidants.Receptor for AGE (RAGE): signaling mechanisms in the pathogenesis of diabetes and its complications.Receptor for advanced glycation end products (RAGE) and implications for the pathophysiology of heart failure.Investigation of phosphoproteome in RAGE signaling.Deoxycholic acid-modified polyethylenimine based nanocarriers for RAGE siRNA therapy in acute myocardial infarction.Etiology-specific assessment of predictors of long-term survival in chronic systolic heart failure Targeting the Receptor for Advanced Glycation Endproducts (RAGE): A Medicinal Chemistry Perspective.Association of serum HMGB2 level with MACE at 1 mo of myocardial infarction: Aggravation of myocardial ischemic injury in rats by HMGB2 via ROS.Hypoxia driven glycation: Mechanisms and therapeutic opportunities.Advanced glycation end products (AGEs) and cardiovascular dysfunction: focus on high molecular weight AGEs.Stopping the primal RAGE reaction in myocardial infarction: capturing adaptive responses to heal the heart?Carbon monoxide form of PEGylated hemoglobin protects myocardium against ischemia/reperfusion injury in diabetic and normal mice.

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RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine model.

http://www.wikidata.org/entity/Q46775210

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RAGE modulates myocardial inju ...... T signaling in a murine model.

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RAGE modulates myocardial inju ...... T signaling in a murine model.

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RAGE modulates myocardial inju ...... T signaling in a murine model.

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RAGE modulates myocardial inju ...... T signaling in a murine model.

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RAGE modulates myocardial inju ...... T signaling in a murine model.

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AJPHEART.01210.2007

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American Journal of Physiology - Heart and Circulatory Physiology

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RAGE modulates myocardial inju ...... T signaling in a murine model.

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P2093

Alexey Aleshin

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Ann Marie Schmidt

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Fei Song

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Matthias Szabolcs

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Qing Li

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Radha Ananthakrishnan

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Ravichandran Ramasamy

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Rosa Rosario

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Rui Liu

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Shi Fang Yan

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P2860

RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides

Inhibition of norepinephrine-induced cardiac hypertrophy in s100beta transgenic mice.

Aldose reductase pathway mediates JAK-STAT signaling: a novel axis in myocardial ischemic injury

Novel cardioprotective role of a small heat-shock protein, Hsp20, against ischemia/reperfusion injury.

Central role of RAGE-dependent neointimal expansion in arterial restenosis.

Cardiomyocyte-restricted knockout of STAT3 results in higher sensitivity to inflammation, cardiac fibrosis, and heart failure with advanced age.

Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts.

RAGE limits regeneration after massive liver injury by coordinated suppression of TNF-alpha and NF-kappaB

RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy.

Anesthetic inhibition in ischemic and nonischemic murine heart: comparison with conscious echocardiographic approach.

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10.1152/AJPHEART.01210.2007

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