Journal article
Silencing of miR-34a attenuates cardiac dysfunction in a setting of moderate, but not severe, hypertrophic cardiomyopathy
BC Bernardo, XM Gao, YK Tham, H Kiriazis, CE Winbanks, JYY Ooi, EJH Boey, S Obad, S Kauppinen, P Gregorevic, XJ Du, RCY Lin, JR McMullen
Plos One | PUBLIC LIBRARY SCIENCE | Published : 2014
Abstract
Therapeutic inhibition of the miR-34 family (miR-34a,-b,-c), or miR-34a alone, have emerged as promising strategies for the treatment of cardiac pathology. However, before advancing these approaches further for potential entry into the clinic, a more comprehensive assessment of the therapeutic potential of inhibiting miR-34a is required for two key reasons. First, miR-34a has ∼40% fewer predicted targets than the miR-34 family. Hence, in cardiac stress settings in which inhibition of miR-34a provides adequate protection, this approach is likely to result in less potential off-target effects. Secondly, silencing of miR-34a alone may be insufficient in settings of established cardiac pathology..
View full abstractGrants
Awarded by National Science Foundation
Funding Acknowledgements
This study was funded by National Health and Medical Research Council Project Grant 586603 (to J.R.M and R.C.Y.L), and also supported in part by the Victorian Government's Operational Infrastructure Support Program. X.J.D. and J.R.M are National Health and Medical Research Council Senior Research Fellows (APP1043026 and 586604). J.R.M, R.C.Y.L., and P. G. are supported by an Australian Research Council Future Fellowship (FT0001657), a University of New South Wales Vice Chancellor Research Fellowship, and a Pfizer Australia Senior Research Fellowship, respectively. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.