Source:http://linkedlifedata.com/resource/pubmed/id/19804286
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2009-10-6
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pubmed:abstractText |
In the normal heart, impulses are generated from the sinoatrial node. It is generally accepted that the pacemaker current, I(f), plays a major role in the spontaneous rhythmic activity. Recently, several electrophysiological and molecular data demonstrate that I(f) channels are present in embryonic and post-natal ventricular myocytes and undergo a downregulation during maturation. Interestingly, the I(f) current is re-expressed in some pathological conditions such as cardiac hypertrophy and heart failure. In these conditions, the overexpression of f-channels is a consequence of electrophysiological remodeling and may represent an arrhythmogenic mechanism in heart failure, a condition associated with high risk for sudden cardiac death. For its physiological and pathophysiological role and the availability of selective f-channel blockers, I(f) may be a suitable therapeutic target in heart failure.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:status |
PubMed-not-MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1744-8298
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
657-66
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pubmed:year |
2007
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pubmed:articleTitle |
I(f) channels as a therapeutic target in heart disease.
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pubmed:affiliation |
University of Florence, Centro Interuniversitario di Medicina Molecolare e Biofisica Applicata (CIMMBA) & Department of Pharmacology, Italy. silvia.suffredini@unifi.it
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pubmed:publicationType |
Journal Article
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