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. 2014 Jul 17;5(7):e1325. doi: 10.1038/cddis.2014.287

Table 1. Summary of miRNAs linked to apoptotic regulation in cardiomyocytes.

miRNAs Relevance to CVD Targets relevant to apoptosis Refs
miR-1 Serum expression upregulated in human AMI and in patients after open-heart surgery with cardiopulmonary bypass PRKCE (protein kinase C) 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159
  Overexpression enhances and inhibition attenuates apoptosis and infarct area after cardiac I/R injury in mice HSPD1 (HSP60)  
  Overexpression inhibits apoptosis in a rat model of cardiac hypertrophy induced by pressure overload BCL2  
  Ischemic post-conditioning upregulates miR-1 and inhibits cardiomyocyte apoptosis in rats    
  Inhibition in vitro in cardiomyocytes reduces H2O2-induced and high-glucose-induced apoptosis    
  Upregulation has pro-apoptotic effect in H9c2 cells exposed to oxidative stress    
  miR-1 transfected ES cells protect host myocardium from MI-induced apoptosis    
  overexpression enhances the angiogenic differentiation of human cardiomyocyte PC    
  Upregulated in rat cardiomyocytes exposed to high glucose    
  Downregulated in response to Tanshinone IIA    
miR-15 family Upregulated in response to MI Silencing in vitro renders cardiomyocytes resistant to hypoxia-induced cell death BCL2 160, 161, 162, 163
  Regulates angiogenic activity of endothelial cells    
miR-133a Upregulation of miR-133a following ischemic post-conditioning CASP9 155, 156, 164, 165
  miR-133a mimic attenuated IR-induced apoptosis in rats    
  Anti-apoptotic effect in H9c2 cells exposed to oxidative stress    
  Elevated levels of miR-133a in patients with ST-elevation myocardial infarction (STEMI) linked to more severe injury    
  Increased expression in Tanshinone IIA-treated hypoxic neonatal cardiomyocytes    
miR-17-92 cluster Overexpression of the cluster results in lethal cardiomyopathy Expression decreases in aging mice hearts   166, 167, 168, 169
  miR-20a is upregulated in mechanically stretched neonatal rat cardiomyocytes and exerts anti-apoptotic effect    
  Overexpression of miR-19b inhibits apoptosis in P19 cells    
miR-21 Myocardial upregulation of miR-21 reduces MI size and apoptotic rate by increasing Bcl-2 levels BCL2 FASLG (FASL) 170, 171, 172, 173, 174, 175, 176
  Expression declines in cardiac myocytes upon exposure to hypoxia, and increases after ischemic preconditioning PDCD4  
  Overexpression diminishes murine coxsackievirus B3-induced myocardiatis ANXA2  
  Overexpression in transgenic mouse heart results in smaller infarct following ischemia SOD2 TXNDAXX  
  Expression elevated in circulating endothelial progenitor cells from diabetic patients and protective from high-glucose-induced apoptosis    
  Expressed in cardiac valve endothelium, where it regulates the development of AV valve    
miR-24 Expression lower in peri-infarct tissue in mouse model of MI BIM 68, 177
  Inhibition induces cardiomyocyte apoptosis    
  In vivo overexpression inhibits cardiomyocyte apoptosis and attenuates infarct size    
  Inhibition enhances EC survival    
miR-30 Inhibits mitochondrial fission and apoptosis in cardiomyocytes TP53 178
miR-150 Upregulated in cardiac myocytes treated with H2O2 MYB (c-myb) 147, 179
  Silencing protects from H2O2-induced apoptosis    
  Dysregulated in human MI    
miR-210 Upregulated in hypoxic cardiomyocytes ? 147, 180
  Overexpression reduces cell death in response to oxidative stress    
  Deregulated in human MI    
miR-199a Downregulated to undetectable levels during cardiac ischemia in vitro and in vivo HIF1A SIRT1 181
  Overexpression inhibits hypoxia-induced expression of several pro-apoptotic genes (e.g. CASP3 and CASP9)    
miR-320 Downregulated in murine hearts following I/R HSPB6 (Hsp20) 182
  Overexpression enhanced cardiomyocyte apoptosis    
miR-149 Overexpression decreases apoptotic sensitivity BBC3 (PUMA) 183
  G-allele of A>G SNP in pre-miR-149 decreases production of miR-149 and influences cardiac function in mouse model of MI    
miR-761 Inhibits mitochondrial fission MFF 62
  Knockdown diminished H2O2-induced and I/R-induced cardiomyocyte apoptosis and infarct size in mice    
miR-499 Inhibits cardiomyocyte apoptosis PPP3CA, PPP3CB 184
miR-214 Protects cardiomyocytes from H2O2-induced apoptosis in vitro PTEN BIM 185, 186
  Genetic deletion in mice increases cardiac apoptosis    
miR-145 Circulating levels reduced in patients with coronary artery disease CAMK2G 67, 187
  Ameliorates ROS-induced apoptosis in cardiomyocytes    
miR-378 Downregulated in a rat model of myocardial ischemia CASP3 188
  Overexpression in H9c2 cardiomyocytes reduces apoptosis and necrosis    
  Inhibition increases H2O2-induced apoptosis    
miR-195 Inhibition leads to decreased ROS production and apoptosis in palmitate-treated mouse cardiomyocytes SIRT1 189
miR-34a Expression increases with aging (in mice) SIRT1 PNUTS 125, 190, 191
  Inhibition reduces cardiomyocyte apoptosis    
  Levels higher in endothelial progenitor cells from coronary artery disease patients    
  Regulates SIRT1 expression in endothelial progenitor cells and contributes to endothelial senescence