TABLE 2.
Direct gene targets of miR‐32 in cardiovascular and metabolic‐related diseases
| Disease | miR‐32 change | Target | Cell lines | In vivo verification | Target function | Reference |
|---|---|---|---|---|---|---|
| AMI | Up | KLF2 | HUVECs | No | Suppress cell viability, pro‐inflammation | Dai et al. (2020)Ref:22 |
| CCSCI | Down | NOTCH‐1 | HUVECs | Yes | Inhibit angiogenesis | Cheng et al. (2020)Ref:29 |
| VC | Up | PTEN | VSMCS | Yes | Inhibit VSMC osteogenic differentiation | Liu et al. (2017)Ref:6 |
| DN | Up | SMAD7 | HK‐2 | Yes | Autophagy suppression, promote fibrosis,EMT and inflammation | Wang et al. (2020b)Ref:13 |
| Cardiac fibrosis | Up | DUSP1 | hCFs | No | Enhance apoptosis and induce the phenotypic alteration | Shen et al. (2019a)Ref:38 |
Abbreviations: AMI, acute myocardial infarction; CAC, coronary artery calcification; CCSCI, chronic compressive spinal cord injury; DN, Diabetic nephropathy; EMT, epithelial‐mesenchymal transition; hCFs, human cardiac fibroblasts; HUVECs, human umbilical vein endothelial cells; PTEN, phosphatase and tensin homolog; VC, vascular calcification; VSMCs, vascular smooth muscle cells.