The role of thyroid hormone nuclear receptors in the heart: evidence from pharmacological approaches.

Abstract:

:This review evaluates the hypothesis that the cardiac effects of amiodarone can be explained-at least partly-by the induction of a local 'hypothyroid-like condition' in the heart. Evidence supporting the hypothesis comprises the observation that amiodarone exerts an inhibitory effect on the binding of T3 to thyroid hormone receptors (TR) alpha-1 and beta-1 in vitro, and on the expression of particular T3-dependent genes in vivo. In the heart, amiodarone decreases heart rate and alpha myosin heavy chain expression (mediated via TR alpha-1), and increases sarcoplasmic reticulum calcium-activated ATPase and beta myosin heavy chain expression (mediated via TR beta-1). Recent data show a significant similarity in expression profiles of 8,435 genes in the heart of hypothyroid and amiodarone-treated animals, although similarities do not always exist in transcripts of ion channel genes. Induction of a hypothyroid cardiac phenotype by amiodarone may be advantageous by decreasing energy demands and increasing energy availability.

journal_name

Heart Fail Rev

journal_title

Heart failure reviews

authors

Wiersinga WM

doi

10.1007/s10741-008-9131-9

subject

Has Abstract

pub_date

2010-03-01 00:00:00

pages

121-4

issue

2

eissn

1382-4147

issn

1573-7322

journal_volume

15

pub_type

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