TY - JOUR
T1 - Therapeutic potential of microRNAs in heart failure
AU - Dorn, Gerald W.
PY - 2010/5
Y1 - 2010/5
N2 - There is an ongoing explosion of information about microRNAs (miRs) in cardiac disease. These small noncoding RNAs regulate protein expression by destabilization and translational inhibition of target mRNAs. Similar to mRNAs, miRs are regulated in cardiac hypertrophy and heart failure, but miR expression profiles appear to be more sensitive than mRNA signatures to changes in clinical status, suggesting that miR levels in myocardium or plasma could enhance clinical diagnostics. Single miRs can target dozens or hundreds of different mRNAs, complicating attempts to determine their individual physiologic effects. However, manipulating individual miRs by overexpression or gene ablation in experimental models has begun to unravel this conundrum: Single miRs tend to regulate numerous effectors within the same functional pathway, producing a coherent physiologic response via multiple parallel perturbations. miRs are attractive nodal therapeutic targets, and stable miR mimetics (agomiRs) and antagonists (antagomiRs) are being evaluated to prevent or reverse heart failure.
AB - There is an ongoing explosion of information about microRNAs (miRs) in cardiac disease. These small noncoding RNAs regulate protein expression by destabilization and translational inhibition of target mRNAs. Similar to mRNAs, miRs are regulated in cardiac hypertrophy and heart failure, but miR expression profiles appear to be more sensitive than mRNA signatures to changes in clinical status, suggesting that miR levels in myocardium or plasma could enhance clinical diagnostics. Single miRs can target dozens or hundreds of different mRNAs, complicating attempts to determine their individual physiologic effects. However, manipulating individual miRs by overexpression or gene ablation in experimental models has begun to unravel this conundrum: Single miRs tend to regulate numerous effectors within the same functional pathway, producing a coherent physiologic response via multiple parallel perturbations. miRs are attractive nodal therapeutic targets, and stable miR mimetics (agomiRs) and antagonists (antagomiRs) are being evaluated to prevent or reverse heart failure.
KW - Cardiac disease
KW - Heart failure
KW - MRNA
KW - MicroRNA
UR - http://www.scopus.com/inward/record.url?scp=77956394522&partnerID=8YFLogxK
U2 - 10.1007/s11886-010-0096-7
DO - 10.1007/s11886-010-0096-7
M3 - Review article
C2 - 20424963
AN - SCOPUS:77956394522
SN - 1523-3782
VL - 12
SP - 209
EP - 215
JO - Current Cardiology Reports
JF - Current Cardiology Reports
IS - 3
ER -