Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-4-19
pubmed:abstractText
Digoxin has been used as an inotropic agent in heart failure for a long time. Troponin I (TnI) phosphorylation is related to cardiac contractility, and the genes are regulated by peroxisome proliferator-activated receptors (PPARs). Our previous studies indicated that cardiac abnormality related to the depressed expression of PPAR? in the hearts of STZ rats is reversed by digoxin. However, the cellular mechanisms for this effect of digoxin have not been elucidated. The aim of the present study was to investigate possible mechanisms for this effect of digoxin using the H9c2 cell line cultured in high glucose (HG) conditions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1476-5381
pubmed:author
pubmed:copyrightInfo
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
pubmed:issnType
Electronic
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
390-8
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Characterization of the mechanisms of the increase in PPAR? expression induced by digoxin in the heart using the H9c2 cell line.
pubmed:affiliation
Department of Cardiology, Chi-Mei Medical Center, Yong Kang City, Tainan County, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't