TY - JOUR
T1 - MicroRNAs
T2 - Novel Molecular Targets and Response Modulators of Statin Therapy
AU - Mohajeri, Mohammad
AU - Banach, Maciej
AU - Atkin, Stephen L.
AU - Butler, Alexandra E.
AU - Ruscica, Massimiliano
AU - Watts, Gerald F.
AU - Sahebkar, Amirhossein
PY - 2018/11/1
Y1 - 2018/11/1
N2 - Cardiovascular disease (CVD) is a major cause of death globally. Addressing cardiovascular risk factors, particularly dyslipidemia, represents the most robust clinical strategy towards reducing the CVD burden. Statins inhibit 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase and represent the main therapeutic approach for lowering cholesterol and reducing plaque formation/rupture. The protective effects of statins extend beyond lowering cholesterol. MicroRNAs (miRNAs or miRs), small noncoding regulatory RNAs, likely mediate the positive pleiotropic effects of statins via modulation of lipid metabolism, enhancement of endothelial function, inhibition of inflammation, improvement of plaque stability, and immune regulation. miRNAs are implicated in statin-related interindividual variations in therapeutic response, directly via HMG-CoA reductase, or indirectly through targeting cytochrome P450 3A (CYP3A) functionality and proprotein convertase subtilisin/kexin type9 (PCSK9) biology.
AB - Cardiovascular disease (CVD) is a major cause of death globally. Addressing cardiovascular risk factors, particularly dyslipidemia, represents the most robust clinical strategy towards reducing the CVD burden. Statins inhibit 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase and represent the main therapeutic approach for lowering cholesterol and reducing plaque formation/rupture. The protective effects of statins extend beyond lowering cholesterol. MicroRNAs (miRNAs or miRs), small noncoding regulatory RNAs, likely mediate the positive pleiotropic effects of statins via modulation of lipid metabolism, enhancement of endothelial function, inhibition of inflammation, improvement of plaque stability, and immune regulation. miRNAs are implicated in statin-related interindividual variations in therapeutic response, directly via HMG-CoA reductase, or indirectly through targeting cytochrome P450 3A (CYP3A) functionality and proprotein convertase subtilisin/kexin type9 (PCSK9) biology.
KW - cardiovascular disease
KW - interindividual variation
KW - microRNAs
KW - pleiotropic effects
KW - Statins
UR - http://www.scopus.com/inward/record.url?scp=85053706503&partnerID=8YFLogxK
U2 - 10.1016/j.tips.2018.09.005
DO - 10.1016/j.tips.2018.09.005
M3 - Review article
C2 - 30249403
AN - SCOPUS:85053706503
SN - 0165-6147
VL - 39
SP - 967
EP - 981
JO - Trends in Pharmacological Sciences
JF - Trends in Pharmacological Sciences
IS - 11
ER -
