Open AccessTGF-β 1 -Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging
Author(s) -
Xiaojin Hao,
Yanmin Zhang,
Xinzhao Zhang,
Mahesh Nirmalan,
Laura Davies,
Dimitrios Konstantinou,
Fei Yin,
Halina Dobrzynski,
Xin Wang,
Andrew A. Grace,
Henggui Zhang,
Mark R. Boyett,
Christopher Huang,
Ming Lei
Publication year - 2011
Publication title -
circulation arrhythmia and electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.684
H-Index - 102
eISSN - 1941-3149
pISSN - 1941-3084
DOI - 10.1161/circep.110.960807
Subject(s) - sinoatrial node , fibrosis , downregulation and upregulation , medicine , knockout mouse , endocrinology , cardiac fibrosis , transforming growth factor , phenotype , biology , gene , heart rate , receptor , genetics , blood pressure
Mutations in the cardiac Na(+) channel gene (SCN5A) can adversely affect electric function in the heart, but effects can be age dependent. We explored the interacting effects of Scn5a disruption and aging on the pathogenesis of sinus node dysfunction in a heterozygous Scn5a knockout (Scn5a(+/-)) mouse model.
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