Source:http://linkedlifedata.com/resource/pubmed/id/12806426
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
2003-6-13
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| pubmed:abstractText |
Erectile dysfunction is a condition that is estimated to affect more than 30 million men in the United States alone. The prevalence of erectile dysfunction is increased with age and is often secondary to diseases such as depression, hypertension and diabetes. Causes of erectile dysfunction include physical injury to the cavernosum and abnormal cerebral and peripheral nervous system functioning. However, many cases of erectile dysfunction are the result of dysfunctional signaling in the cavernosal vasculature. This article will detail the important role of a vasoconstrictor mechanism mediated by the small G-protein RhoA and a downstream serine/threonine kinase, Rho-kinase, in the maintenance of penile flaccidity. Recent evidence demonstrates that inhibition of endogenous Rho-kinase initiates an erectile response in an in vivo rat model. These initial findings introduce a novel potential therapeutic approach for the treatment of erectile dysfunction.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:status |
PubMed-not-MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0214-0934
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| pubmed:author | |
| pubmed:copyrightInfo |
(c) 2001 Prous Science. All rights reserved.
|
| pubmed:issnType |
Print
|
| pubmed:volume |
14
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
601-6
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| pubmed:year |
2001
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| pubmed:articleTitle |
Rho-kinase as a potential target for the treatment of erectile dysfunction.
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| pubmed:affiliation |
Dept. of Physiology, University of Michigan, Ann Arbor, Michigan, USA.
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| pubmed:publicationType |
Journal Article
|