Linked Life Data

17663674

Source:http://linkedlifedata.com/resource/pubmed/id/17663674

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
156
pubmed:dateCreated
2007-7-31
pubmed:abstractText
In the 1960s, serotonin (5HT) was associated with pulmonary arterial hypertension (PAH) caused by certain diet pills, but has recently been the subject of renewed interest in the field of PAH. Serotonin can be synthesised in the pulmonary endothelium with the rate-limiting step being the activity of tryptophan hydroxylase1 (Tph1). The serotonin is released and can then: (i) pass into the underlying pulmonary smooth muscle cells through the serotonin transporter (SERT) to initiate proliferation and/or (ii) activate serotonin receptors on pulmonary smooth muscle cells to evoke proliferation and/or contraction. Serotonin may also mediate pulmonary fibroblast proliferation via the SERT and/or serotonin receptors. Here we will unravel, discuss and update the 'serotonin hypothesis' of PAH in light of recent advances in the field. In conclusion, the activity of serotonin receptors, the SERT and Tph1 can all be elevated in clinical and experimental PAH and each offers a potentially unique therapeutic target.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1368-504X
pubmed:author
pubmed:issnType
Print
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
27-31
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Pulmonary hypertension and the serotonin hypothesis: where are we now?
pubmed:affiliation
Division of Neuroscience and Biomedical Systems, University of Glasgow, Glasgow, UK. m.maclean@bio.gla.ac.uk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't