Table 2.
Summary of studies with association between the 27 selected miRNAs and heart disease
| miRNAs | Ref. | Description |
|---|---|---|
| miR-451 | [39] | Upregulated in heart due to ischemia |
| miR-22 | [40] | Elevated serum levels in patients with stablechronic systolic heart failure |
| miR-133 | [41] | Downregulated in transverse aortic constrictionand isoproterenol-induced hypertrophy |
| miR-709 | [42] | Upregulated in rat heart four weeks after chronicdoxorubicin treatment |
| miR-126 | [43] | Association with outcome of ischemic andnonischemic cardiomyopathy in patients withchronic heart failure |
| miR-30 | [44] | Inversely related to CTGF in two rodent modelsof heart disease, and human pathological leftventricular hypertrophy |
| miR-29 | [45] | Downregulated in the heart region adjacent toan infarct |
| miR-143 | [46] | Molecular key to switching of the vascular smoothmuscle cell phenotype that plays a critical role incardiovascular disease pathogenesis |
| miR-24 | [47] | Regulates cardiac fibrosis after myocardial infarction |
| miR-23 | [48] | Upregulated during cardiac hypertrophy |
| miR-378 | [49] | Cardiac hypertrophy control |
| miR-125 | [50] | Important regulator of hESC differentiation to cardiacmuscle(potential therapeutic application) |
| miR-675 | [51] | Elevated in plasma of heart failure patients |
| let-7 | [52] | Aberrant expression of let-7 members incardiovascular disease |
| miR-16 | [53] | Circulating prognostic biomarker in critical limbischemia |
| miR-26 | [54] | Downregulated in a rat cardiac hypertrophy model |
| miR-669 | [55] | Prevents skeletal muscle differentiation in postnatalcardiac progenitors |