Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 1
pubmed:dateCreated
2004-4-14
pubmed:abstractText
Proteasomes are the main non-lysosomal, multicatalytic proteinase complexes involved in the degradation of most intracellular proteins and in numerous cell processes. Studies from isolated cell models indicate that agents that induce oxidative stress may also damage proteasomes. Similarly, continuous oxidative stress during cell aging may impair proteasome activity. In ischemia-reperfusion models of organ injury, proteasomes may be involved in several ways. First, proteasomes were found to be targets of ischemia-reperfusion injury of the brain and heart. Second, proteasome activity increased in liver models of ischemia-reperfusion. Third, proteasome inhibition prevented ischemia-reperfusion injury of the brain, heart and kidney. A major mechanism by which proteasome inhibitors may confer tissue protection is inactivation of transcription activator nuclear factor-kappaB resulting in a block of expression of cytokines and cell adhesion molecules during the reperfusion phase. Thus, proteasome inhibition represents a novel strategy for the treatment of pathologies such as stroke, infarction, and kidney failure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0867-5910
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3-15
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Emerging roles of proteasomes in ischemia-reperfusion injury of organs.
pubmed:affiliation
Laboratory of Perfused Organs, SCOT, Slovak Medical University - Institute of Preventive and Clinical Medicine, Bratislava, Slovakia. kukan@upkm.sk
pubmed:publicationType
Journal Article, Review