Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
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MicroRNA dysregulation in diabetic ischemic heart failure patientsDiabetic Cardiovascular Disease Induced by Oxidative StressOver-nutrition and metabolic cardiomyopathyNADPH oxidases in heart failure: poachers or gamekeepers?Cardiac dysfunction and oxidative stress in the metabolic syndrome: an update on antioxidant therapiesHigh glucose-mediated oxidative stress impairs cell migration.Increased propensity for cell death in diabetic human heart is mediated by mitochondrial-dependent pathwaysTherapeutic inhibition of mitochondrial reactive oxygen species with mito-TEMPO reduces diabetic cardiomyopathyMitochondrial Calpain-1 Disrupts ATP Synthase and Induces Superoxide Generation in Type 1 Diabetic Hearts: A Novel Mechanism Contributing to Diabetic CardiomyopathyMolecular mechanistic associations of human diseasesInhibition of calpain reduces oxidative stress and attenuates endothelial dysfunction in diabetes.Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy.Novel aspects of the roles of Rac1 GTPase in the cardiovascular systemDeficiency of a lipid droplet protein, perilipin 5, suppresses myocardial lipid accumulation, thereby preventing type 1 diabetes-induced heart malfunctionDeficiency of rac1 blocks NADPH oxidase activation, inhibits endoplasmic reticulum stress, and reduces myocardial remodeling in a mouse model of type 1 diabetes.Diabetic cardiomyopathy, causes and effects.Tiam1/Rac1 signaling pathway mediates palmitate-induced, ceramide-sensitive generation of superoxides and lipid peroxides and the loss of mitochondrial membrane potential in pancreatic beta-cells.Hyperglycaemia-induced cardiomyocyte death is mediated via MCP-1 production and induction of a novel zinc-finger protein MCPIP.Resveratrol-enhanced autophagic flux ameliorates myocardial oxidative stress injury in diabetic mice.Retinoic acid receptor-mediated signaling protects cardiomyocytes from hyperglycemia induced apoptosis: role of the renin-angiotensin systemFriendly, and not so friendly, roles of Rac1 in islet β-cell function: lessons learnt from pharmacological and molecular biological approachesMicroRNAs involved in the mitogen-activated protein kinase cascades pathway during glucose-induced cardiomyocyte hypertrophy.EHT 1864, a small molecule inhibitor of Ras-related C3 botulinum toxin substrate 1 (Rac1), attenuates glucose-stimulated insulin secretion in pancreatic β-cells.Increased phagocyte-like NADPH oxidase and ROS generation in type 2 diabetic ZDF rat and human islets: role of Rac1-JNK1/2 signaling pathway in mitochondrial dysregulation in the diabetic islet.Updating experimental models of diabetic cardiomyopathyHeat stress induced apoptosis is triggered by transcription-independent p53, Ca(2+) dyshomeostasis and the subsequent Bax mitochondrial translocation.Silencing of miR-195 reduces diabetic cardiomyopathy in C57BL/6 miceHistone deacetylase (HDAC) inhibition improves myocardial function and prevents cardiac remodeling in diabetic mice.Cluster Differentiating 36 (CD36) Deficiency Attenuates Obesity-Associated Oxidative Stress in the Heart.Deficiency of Capn4 gene inhibits nuclear factor-κB (NF-κB) protein signaling/inflammation and reduces remodeling after myocardial infarction.Cardiomyocyte-specific overexpression of an active form of Rac predisposes the heart to increased myocardial stunning and ischemia-reperfusion injuryCurcumin Protects Neonatal Rat Cardiomyocytes against High Glucose-Induced Apoptosis via PI3K/Akt Signalling PathwayInhibition of MicroRNA 195 Prevents Apoptosis and Multiple-Organ Injury in Mouse Models of Sepsis.Inhibition of Rac1 reduces store overload-induced calcium release and protects against ventricular arrhythmiaSodium-myoinositol cotransporter-1, SMIT1, mediates the production of reactive oxygen species induced by hyperglycemia in the heart.Therapeutic properties of Scutellaria baicalensis in db/db mice evaluated using Connectivity Map and network pharmacology.NADPH oxidases and cardiac remodelling.Diabetic Cardiomyopathy: Mechanisms and Therapeutic Targets.Role of Rac1-mineralocorticoid-receptor signalling in renal and cardiac disease.ALDH2 Inhibition Potentiates High Glucose Stress-Induced Injury in Cultured Cardiomyocytes.
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Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
description
article científic
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article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on 10 July 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
@en
Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
@nl
type
label
Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
@en
Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
@nl
prefLabel
Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
@en
Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
@nl
P2093
P2860
P356
P1433
P1476
Rac1 is required for cardiomyocyte apoptosis during hyperglycemia.
@en
P2093
Huaqing Zhu
J Malcolm O Arnold
Limei Shan
Qingping Feng
Tianqing Peng
P2860
P304
P356
10.2337/DB08-0617
P407
P577
2009-07-10T00:00:00Z