Linked Life Data

19347338

Source:http://linkedlifedata.com/resource/pubmed/id/19347338

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-6-10
pubmed:abstractText
Patients with insulin resistance and early type 2 diabetes exhibit an increased propensity to develop a diffuse and extensive pattern of arteriosclerosis. Diabetic subjects show a remarkable increase in vascular complications, including myocardial infarction and strokes. The accelerated atherosclerosis in these patients is likely to be multifactorial. In this review, we focus on the advanced glycation end product (AGE)-receptor for AGE (RAGE) axis and the role of C-peptide as a mediator of lesion development. AGEs are proteins or lipids that become glycated after exposure to sugars. By engaging the RAGEs, AGEs induce the expression of proinflammatory mediators in various vascular cell types and are involved in a variety of microvascular and macrovascular complications. In animal models, interruption of the AGE-RAGE interaction reduces lesion size and plaque development and RAGE deficiency in a RAGE(-/-)/apolipoprotein E(-/-) double knockout mouse attenuates the development of atherosclerosis in diabetes. On the other side, patients with type 2 diabetes show increased levels of C-peptide and over the last years various groups examined the effect of C-peptide in vascular cells as well as its potential role in lesion development. Recent data suggest that the proinsulin cleavage product C-peptide could play a causal role in atherogenesis by promoting monocyte and CD4-positive lymphocyte recruitment in early arteriosclerotic lesions and by inducing the proliferation of vascular smooth muscle cells. The following review will summarize these two pathophysiological aspects and discuss on the one hand the potential role of the activated AGE-RAGE axis in diabetes-accelerated atherogenesis and on the other hand the role of C-peptide as a mediator in lesion development in patients with type 2 diabetes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1863-2300
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
103-11
pubmed:dateRevised
2011-10-28
pubmed:meshHeading
pubmed-meshheading:19347338-Animals, pubmed-meshheading:19347338-Antigens, Neoplasm, pubmed-meshheading:19347338-Apolipoproteins E, pubmed-meshheading:19347338-Atherosclerosis, pubmed-meshheading:19347338-C-Peptide, pubmed-meshheading:19347338-CD4-Positive T-Lymphocytes, pubmed-meshheading:19347338-Cell Proliferation, pubmed-meshheading:19347338-Diabetes Mellitus, Type 2, pubmed-meshheading:19347338-Diabetic Angiopathies, pubmed-meshheading:19347338-Gene Expression Regulation, pubmed-meshheading:19347338-Glycosylation End Products, Advanced, pubmed-meshheading:19347338-Humans, pubmed-meshheading:19347338-Inflammation Mediators, pubmed-meshheading:19347338-Mice, pubmed-meshheading:19347338-Mice, Knockout, pubmed-meshheading:19347338-Mitogen-Activated Protein Kinases, pubmed-meshheading:19347338-Monocytes, pubmed-meshheading:19347338-Myocardial Infarction, pubmed-meshheading:19347338-Myocytes, Smooth Muscle, pubmed-meshheading:19347338-Stroke
pubmed:year
2009
pubmed:articleTitle
Advanced glycation end products and C-peptide-modulators in diabetic vasculopathy and atherogenesis.
pubmed:affiliation
Department of Internal Medicine II-Cardiology, University of Ulm, Robert-Koch-Str. 8, 89081, Ulm, Germany.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't