Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
1999-10-8
pubmed:abstractText
The Diabetes Control and Complications Trial (DCCT) established the importance of hyperglyemia and other consequences of insulin deficiency in the pathogenesis of diabetic neuropathy, but the precise mechanisms by which metabolic alterations produce peripheral nerve fiber damage and loss remain unclear. Emerging data from human and animal studies suggest that glucose-derived oxidative stress may play a central role, linking together many of the other currently invoked pathogenetic mechanisms such as the aldose reductase and glycation pathways, vascular dysfunction, and impaired neurotrophic support. These relationships suggest combinations of pharmacological interventions that may synergistically protect the peripheral nervous system (PNS) against the metabolic derangements of diabetes mellitus.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
375
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
217-23
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Glucose-induced oxidative stress and programmed cell death in diabetic neuropathy.
pubmed:affiliation
Department of Internal Medicine, and Michigan Diabetes Research and Training Center, University of Michigan, Ann Arbor, USA. dgreene@umich.edu
pubmed:publicationType
Journal Article, Review