Advanced glycation end product cross-link breaker attenuates diabetes-induced cardiac dysfunction by improving sarcoplasmic reticulum calcium handling. - Wikidata - awgldk - TriplyDB

Advanced glycation end product cross-link breaker attenuates diabetes-induced cardiac dysfunction by improving sarcoplasmic reticulum calcium handling.

Advanced glycation end product cross-link breaker attenuates diabetes-induced cardiac dysfunction by improving sarcoplasmic reticulum calcium handling.

http://www.wikidata.org/entity/Q36193769

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How exercise may amend metabolic disturbances in diabetic cardiomyopathy Expression and regulation of facilitative glucose transporters in equine insulin-sensitive tissue: from physiology to pathology.Hyperinsulinemia Down-Regulates TLR4 Expression in the Mammalian Heart.Targeting metabolic disturbance in the diabetic heart.Diabetes Alters the Expression and Translocation of the Insulin-Sensitive Glucose Transporters 4 and 8 in the Atria.The vascular endothelium in diabetes--a therapeutic target?Biomolecular basis of the role of diabetes mellitus in osteoporosis and bone fractures IL-1β, RAGE and FABP4: targeting the dynamic trio in metabolic inflammation and related pathologies.Molecular mechanisms of diabetic cardiomyopathy.Diabetic Cardiomyopathy: An Immunometabolic Perspective.Advanced glycation end products: role in pathology of diabetic cardiomyopathy.Cardiac Physiology of Aging: Extracellular Considerations.Damaging effects of hyperglycemia on cardiovascular function: spotlight on glucose metabolic pathways.Targeting advanced glycation with pharmaceutical agents: where are we now?Pathophysiological Fundamentals of Diabetic Cardiomyopathy.Advanced glycation end products (AGEs) and cardiovascular dysfunction: focus on high molecular weight AGEs.Depressed calcium-handling proteins due to endoplasmic reticulum stress and apoptosis in the diabetic heart are attenuated by argirein.Functional Effects of Alagebrium (ALT-711)-Isolated Rat Carotid Artery.Quantification of Cell-Surface Glucose Transporters in the Heart Using a Biotinylated Photolabeling Assay.Erythropoietin Attenuates Cardiac Dysfunction in Rats by Inhibiting Endoplasmic Reticulum Stress-Induced Diabetic Cardiomyopathy.Molecular mechanism of diabetic cardiomyopathy and modulation of microRNA function by synthetic oligonucleotides.Calcium Signaling in the Ventricular Myocardium of the Goto-Kakizaki Type 2 Diabetic Rat.

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P2860

Advanced glycation end product cross-link breaker attenuates diabetes-induced cardiac dysfunction by improving sarcoplasmic reticulum calcium handling.

http://www.wikidata.org/entity/Q36193769

description

2012 nî lūn-bûn

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2012年論文

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2012年論文

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Advanced glycation end product ...... ic reticulum calcium handling.

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Advanced glycation end product ...... ic reticulum calcium handling.

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FPHYS.2012.00292

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Frontiers in Physiology

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Advanced glycation end product ...... ic reticulum calcium handling.

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Allyson L Kranstuber

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

Brandon J Biesiadecki

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

Carlos Del Rio

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

Joseph Ottobre

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

Robert L Hamlin

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

Sandor Gyorke

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

Véronique A Lacombe

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

P2860

Therapeutic potential of breakers of advanced glycation end product-protein crosslinks

Cardiac excitation-contraction coupling

Advanced glycation end-product cross-link breakers. A novel approach to cardiovascular pathologies related to the aging process

Dyssynchronous (non-uniform) Ca2+ release in myocytes from streptozotocin-induced diabetic rats

Diabetes increases formation of advanced glycation end products on Sarco(endo)plasmic reticulum Ca2+-ATPase.

Chronic diabetes increases advanced glycation end products on cardiac ryanodine receptors/calcium-release channels.

Advanced glycation endproduct (AGE) accumulation and AGE receptor (RAGE) up-regulation contribute to the onset of diabetic cardiomyopathy.

The cross-link breaker, N-phenacylthiazolium bromide prevents vascular advanced glycation end-product accumulation.

Abnormal intrastore calcium signaling in chronic heart failure.

A cross-link breaker has sustained effects on arterial and ventricular properties in older rhesus monkeys

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scholarly article

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10.3389/FPHYS.2012.00292

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3

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230763830

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22934044

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3429064

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