Journal
PHARMACOGENOMICS
Volume 15, Issue 8, Pages 1159-1168Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/PGS.14.76
Keywords
apoptosis; cardiac fibrosis; CRT; HF; hypertrophy; microRNA; responder patients
Categories
Funding
- American Heart Association [AHA13POST16810041]
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Heart failure (HF) disease progression is related to numerous adaptive processes including cardiac fibrosis, hypertrophy and apoptosis by activation of the 'fetal' gene program and downregulation of mRNA signatures, suggesting the importance of molecular mechanisms that suppress nnRNA steady-state levels. miRNAs (miRs) are small, noncoding RNAs that bind mRNAs at their 3'-UTRs, leading to nnRNA degradation or inhibition of protein translation. Several miRs are unregulated in response to cellular stress and can modify cellular functions such as proliferation, differentiation and programmed death; these miRs are also regulated in cardiac disease. Cardiac resynchronization therapy improves cardiac performance and myocardial mechanical efficiency. In this updated critical appraisal we report on the main miRs that play a key role in response to cardiac resynchronization therapy (i.e., responder vs nonresponder HF patients), focusing on the miR-mediated modulation of cardiac angiogenesis, apoptosis, fibrosis and membrane ionic currents.
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