Linked Life Data

17934656

Source:http://linkedlifedata.com/resource/pubmed/id/17934656

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-10-15
pubmed:abstractText
The determinant of the diabetic nephropathy is hyperglycemia, but hypertension and other genetic factors are also involved. Glomerulus is the focus of the injury, where mesangial cell proliferation and extracellular matrix occur because of the increase of the intra- and extracellular glucose concentration and overexpression of GLUT1. Sequentially, there are increases in the flow by the poliol pathway, oxidative stress, increased intracellular production of advanced glycation end products (AGEs), activation of the PKC pathway, increase of the activity of the hexosamine pathway, and activation of TGF-beta1. High glucose concentrations also increase angiotensin II (AII) levels. Therefore, glucose and AII exert similar effects in inducing extracellular matrix formation in the mesangial cells, using similar transductional signal, which increases TGF-beta1 levels. In this review we focus in the effect of glucose and AII in the mesangial cells in causing the events related to the genesis of diabetic nephropathy. The alterations in the signal pathways discussed in this review give support to the observational studies and clinical assays, where metabolic and antihypertensive controls obtained with angiotensin-converting inhibitors have shown important and additive effect in the prevention of the beginning and progression of diabetic nephropathy. New therapeutic strategies directed to the described intracellular events may give future additional benefits.
pubmed:language
por
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0004-2730
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
901-12
pubmed:meshHeading
pubmed-meshheading:17934656-Angiotensin II, pubmed-meshheading:17934656-Cell Proliferation, pubmed-meshheading:17934656-Diabetic Nephropathies, pubmed-meshheading:17934656-Endothelium-Dependent Relaxing Factors, pubmed-meshheading:17934656-Extracellular Matrix, pubmed-meshheading:17934656-Glomerular Mesangium, pubmed-meshheading:17934656-Glucose Transporter Type 1, pubmed-meshheading:17934656-Glycosylation End Products, Advanced, pubmed-meshheading:17934656-Humans, pubmed-meshheading:17934656-Hyperglycemia, pubmed-meshheading:17934656-Nitric Oxide, pubmed-meshheading:17934656-Oxidative Stress, pubmed-meshheading:17934656-Renin-Angiotensin System, pubmed-meshheading:17934656-Sclerosis, pubmed-meshheading:17934656-Transforming Growth Factor beta1, pubmed-meshheading:17934656-Vasoconstrictor Agents
pubmed:year
2007
pubmed:articleTitle
[Molecular bases of diabetic nephropathy].
pubmed:affiliation
Laboratório de Hipertensão Experimental, Unidade de Hipertensão, Instituto do Coração, HC-FMUSP, São Paulo.
pubmed:publicationType
Journal Article, English Abstract, Review, Research Support, Non-U.S. Gov't