Letter to the Editor

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RBM20 is an essential factor for thyroid hormone-regulated titin isoform transition Free
Chaoqun Zhu1,†, Zhiyong Yin1,2,†, Jun Ren3, Richard J. McCormick1, Stephen P. Ford1, and Wei Guo1,3,*
1Department of Animal Science, College of Agriculture and Natural Resources, University of Wyoming, Laramie, WY 82071, USA
2Department of Cardiology, Xi Jing Hospital, Fourth Military Medical University, Xi'an 710032, China
3Center for Cardiovascular Research and Alternative Medicine, College of Health Science, University of Wyoming, Laramie, WY 82071, USA *Correspondence to:Wei Guo, E-mail: wguo3@uwyo.edu
J Mol Cell Biol, Volume 7, Issue 1, February 2015, Pages 88-90  https://doi.org/10.1093/jmcb/mjv002

Diastolic heart failure (DHF) and systolic heart failure (SHF) are two main subsets of chronic heart failure that are commonly encountered in clinical practice (Chatterjee and Massie, 2007). Although there have been considerable advances in the treatment of SHF, the molecular and biochemical mechanisms mediating the structural remodeling and principal functional derangement in both SHF and DHF remain unclear. In particular, effective therapeutic regimens are still lacking for DHF; thus, it is imperative to better understand the molecular and biochemical mechanisms of DHF in an effort to seek novel therapeutic avenues for patients suffering from DHF. DHF is manifested by stiffer ventricular walls, while SHF has overly compliant ventricular walls. Therefore, altering ventricular wall stiffness will be a potential therapeutic strategy for both DHF and SHF.