Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-8-6
pubmed:abstractText
Mechanisms that lead to cachexia are still poorly understood. The neurohormonal changes that occur in severe disease states may cause an imbalance between protein synthesis and degradation at the cellular level, followed by muscle wasting. Here, we review actions of angiotensin II, TNF-alpha, corticosteroids, insulin-like growth factor-I (IGF-I), and the IGF binding proteins, factors that may each contribute to the metabolic imbalance. The complex endocrine, autocrine and intracellular interactions between these factors will be described with examples from patient, rat and cell culture studies. Moreover, some of the data supporting that each of these hormones may directly affect cellular protein degradation mechanisms will be reviewed. Knowledge on these regulatory mechanisms will facilitate the development of new pharmaceutical strategies to treat cachexia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0167-5273
pubmed:author
pubmed:issnType
Print
pubmed:volume
85
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
111-21, discussion 121-4
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Neurohormonal factors in the development of catabolic/anabolic imbalance and cachexia.
pubmed:affiliation
Division of Cardiology, Fondation pour Recherches Médicales, 64 Ave. de la Roseraie, CH-1205 Geneva, Switzerland. marijke.brink@dim.hcuge.ch
pubmed:publicationType
Journal Article, Review