Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-2-18
pubmed:abstractText
The glomerular response to injury displays astonishingly uniform features that include infiltration with professional immune cells, activation and proliferation of resident glomerular cells and matrix expansion. Cross-communication of intrinsic mesangial cells with invading immune cells is crucial for the fate of glomerular injury: progression to glomerulosclerosis or resolution and repair. The formation of free radicals, particularly of nitric oxide and superoxide, are key events that initiate redox-based signal transduction and gene expression. The balance between these radicals constitutes redox-operated genetic switches that ensure self-limited inflammatory responses to tissue injury. The aberrant production of the mediators, however, may sustain matrix accumulation and result in irreversible alteration of glomerular structure and function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
809-15
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Changing gears in the course of glomerulonephritis by shifting superoxide to nitric oxide-dominated chemistry.
pubmed:affiliation
Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt/Main, Germany. pfielschifter@em.uni-frankfurt.de
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't