Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-10-6
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.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:month
Nov
pubmed:issn
1744-8298
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
657-66
pubmed:year
2007
pubmed:articleTitle
I(f) channels as a therapeutic target in heart disease.
pubmed:affiliation
University of Florence, Centro Interuniversitario di Medicina Molecolare e Biofisica Applicata (CIMMBA) & Department of Pharmacology, Italy. silvia.suffredini@unifi.it
pubmed:publicationType
Journal Article