Open AccessHMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome
Author(s) -
Nerea Hermida,
Andreas Markl,
Julien Hamelet,
Tim Van Assche,
Annelies Vanderper,
Paul Herijgers,
Marc van Bilsen,
Denise HilfikerKleiner,
Gauthier Noppe,
Christophe Beauloye,
Sandrine Horman,
JeanLuc Balligand
Publication year - 2013
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvt070
Subject(s) - diastole , medicine , fibrosis , myocardial fibrosis , metabolic syndrome , cardiac fibrosis , cardiology , endocrinology , amp activated protein kinase , statin , hmg coa reductase , protein kinase a , ampk , reductase , kinase , blood pressure , enzyme , biology , obesity , biochemistry
The metabolic syndrome (MS) leads to myocardial fibrosis (MF) and diastolic dysfunction. Statins have proven beneficial effects in MS, but their impact on cardiac remodelling is uncertain. We examined the effects and mechanisms of chronic statin treatment on cardiac remodelling, e.g. fibrosis and diastolic properties.
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