The heart is a principal target of
thyroid hormone, and a reduction of cardiac
thyroid hormone signaling is thought to play a role in pathological
ventricular remodeling and the development of
heart failure. Studies in various rodent models of
heart disease have identified increased activity of cardiac
type III deiodinase as a possible cause of diminished levels and action of
thyroid hormone. Recent data indicate novel mechanisms underlying the induction of this
thyroid hormone-degrading
enzyme in the heart as well as post-transcriptional regulation of its expression by
microRNAs. In addition, the relevance of diminished
thyroid hormone signaling for cardiac remodeling is suggested to include
miRNA-mediated effects on pathological signaling pathways. These and other recent studies are reviewed and discussed in the context of other processes and factors that have been implicated in the reduction of cardiac
thyroid hormone signaling in
heart failure.