Noncoding RNAs in Ischemic Cardiovascular Disease and Repair Mechanisms
Ischemic cardiomyopathy is frequently a consequence of myocardial infarction resulting in a marked loss of cardiomyocytes, which is replaced by a scar. As endogenous cardiovascular repair mechanisms are not sufficient to compensate for the loss of heart muscle and subsequent adverse remodeling predisposes to development of heart failure, novel experimental therapies are intensely explored to reduce scar size, counteract adverse hypertrophy and promote repair of the heart muscle. These therapies include cell-based therapies, cardiomyo- cytes renewal or proliferation and trans-differentiation into cardiomyocytes. Importantly, microRNAs evolved as major modulators of pathophysiological mechanisms involved in heart failure progression as well as repair mechanisms. Identification of microRNAs contributing or counteracting these deteriorative mechanisms resulted in novel microRNA-targeted therapies in experimental studies. While this class of non-coding RNAs has already entered clinical translation, another subclass of non-coding RNAs - long-non-coding RNAs (lncRNAs) - is now intensely explored as well. Recent observations indicate that lncRNAs are important regulators of cardiovascular development and mechanisms involved
U. Landmesser (*) • P. Jakob
© Springer International Publishing AG 2017
T Thum, S. Dimmeler (eds.), Non-coding RNAs in the Vasculature, Cardiac and Vascular Biology, DOI 10.1007/978-3-319-52945-5_4
in adverse cardiac remodeling and development of cardiomyopathy. Therefore lncRNAs, in addition to microRNAs, may also emerge as novel therapeutic targets in cardiovascular disease.