Linked Life Data

16935841

Source:http://linkedlifedata.com/resource/pubmed/id/16935841

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2006-11-19
pubmed:abstractText
Oxidative stress plays a key role in the pathogenesis of diabetic cardiomyopathy, which is characterized by myocyte loss and fibrosis, finally resulting in heart failure. The study looked at the downstream signaling whereby oxidative stress leads to reduced myocardial contractility in the left ventricle of diabetic rats and the effects of dehydroepiandrosterone (DHEA), which production is suppressed in the failing heart and prevents the oxidative damage induced by hyperglycemia in several experimental models. DHEA was given orally at a dose of 4 mg/rat per day for 21 d to rats with streptozotocin (STZ)-induced diabetes and genetic diabetic-fatty (ZDF) rats. Oxidative balance, advanced glycated end products (AGEs) and AGE receptors, cardiac myogenic factors, and myosin heavy-chain gene expression were determined in the left ventricle of treated and untreated STZ-diabetic rats and ZDF rats. Oxidative stress induced by chronic hyperglycemia increased AGE and AGE receptors and led to activation of the pleoitropic transcription factor nuclear factor-kappaB. Nuclear factor-kappaB activation triggered a cascade of signaling, which finally led to the switch in the cardiac myosin heavy-chain (MHC) gene expression from the alpha-MHC isoform to the beta-MHC isoform. DHEA treatment, by preventing the activation of the oxidative pathways induced by hyperglycemia, counteracted the enhanced AGE receptor activation in the heart of STZ-diabetic rats and ZDF rats and normalized downstream signaling, thus avoiding impairment of the cardiac myogenic factors, heart autonomic nervous system and neural crest derivatives (HAND) and myogenic enhancer factor-2, and the switch in MHC gene expression, which are the early events in diabetic cardiomyopathy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5967-74
pubmed:meshHeading
pubmed-meshheading:16935841-Animals, pubmed-meshheading:16935841-Dehydroepiandrosterone, pubmed-meshheading:16935841-Diabetes Mellitus, Experimental, pubmed-meshheading:16935841-Glycosylation End Products, Advanced, pubmed-meshheading:16935841-Heart, pubmed-meshheading:16935841-Heart Ventricles, pubmed-meshheading:16935841-Male, pubmed-meshheading:16935841-Myocardium, pubmed-meshheading:16935841-Myosin Heavy Chains, pubmed-meshheading:16935841-Organ Specificity, pubmed-meshheading:16935841-Oxidative Stress, pubmed-meshheading:16935841-Rats, pubmed-meshheading:16935841-Rats, Wistar, pubmed-meshheading:16935841-Rats, Zucker, pubmed-meshheading:16935841-Receptors, Immunologic, pubmed-meshheading:16935841-Receptors, Tumor Necrosis Factor, Type I, pubmed-meshheading:16935841-Transcription Factors, pubmed-meshheading:16935841-Tumor Necrosis Factor-alpha
pubmed:year
2006
pubmed:articleTitle
Oxidative stress-dependent impairment of cardiac-specific transcription factors in experimental diabetes.
pubmed:affiliation
Department of Experimental Medicine and Oncology, General Pathology Section, University of Turin, 10126 Turin, Italy.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't