Role of MicroRNAs in Cardiovascular Disease: Therapeutic... : Journal of Cardiovascular Pharmacology (original) (raw)
Invited Review Article
Role of MicroRNAs in Cardiovascular Disease: Therapeutic Challenges and Potentials
From the *Department of Medicine, Division of Cardiology; and †Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO.
Received for publication July 1, 2010; accepted August 5, 2010.
Supported by National Institutes of Health Grants HL051239, HL101435 (J.D.P.), National Institutes of Health Grants HL088708, HL097123 (C.S.).
The authors report no conflicts of interest.
Reprints: J. David Port, PhD, Department of Medicine, Division of Cardiology, University of Colorado School of Medicine, B139, 12700 East 19th Avenue, Aurora, CO 80045 (e-mail: [email protected]).
Abstract
MicroRNAs (miRNAs, miRs) are short approximately 22-nucleotide noncoding RNAs that bind to messenger RNA transcripts and in doing so modulate cognate gene expression. In eukaryotes, miRNAs act primarily by causing translational repression although they may also act to destabilize RNA transcripts. During the past few years, a number of studies have demonstrated that miR expression changes as a result of cardiac hypertrophy or heart failure. Additionally, cell-based and transgenic mouse studies have demonstrated that individual miRs can affect a number of aspects of cardiac biology including developmental processes, stem cell differentiation, progression of hypertrophy and failure, ion channel function, as well as angiogenesis, rates of apoptosis, and fibroblast proliferation. In this review, we will summarize several of the miRs known to change in expression in association with heart failure and outline details of what is known about their putative targets. In addition, we will review several aspects of regulation of miR expression that have not been addressed in a cardiovascular context. Finally, as is common to all new and rapidly moving fields, we will highlight some of the gaps and inconsistencies related to miR expression and cardiac phenotypes, particularly those associated with heart failure.
© 2010 Lippincott Williams & Wilkins, Inc.