Antidiabetic drugs and ncRNAs | |||
---|---|---|---|
Reference | Study Population/experimental system | Treatment | Main findings |
[333] | Mouse liver | Mice treated with metformin | Metformin induced the expression of miR-20a-5p, miR-34a-5p, miR-130a-3p, miR-106b-5p, miR-125b-3p, and let-7c |
[334] | BJ-1s human neonatal foreskin fibroblasts | Cells treated with metformin at different passages | Metformin induced the expression of miR-200a, miR-141, miR-429 and of miR-205 in senescent BJ-1s cells |
[335] | Human umbilical vein ECs | Cells treated with metformin at different passages | Metformin induced the expression of miR-100-5p, miR-125b-5p, miR-654-3p, miR-217 and miR-216a-3p/5p in senescent ECs |
[270] | Mouse bone marrow-derived endothelial precursor cells | Cells treated with palmitic acid and metformin | Metformin reverted angiogenesis impairment caused by palmitic acid by attenuating miR-130a/p-AKT axis and increasing PTEN expression |
[336] | Mouse microvascular ECs | Cells exposed to HG and treated with metformin | Metformin reduced and increased miR-34a-5p and SIRT1 expression levels, respectively, attenuating HG-induced angiogenesis impairment |
[337] | Neonatal rat ventricular cells | Cells exposed to H2O2 and treated with metformin | Metformin reverted H2O2- and ischemia/reperfusion-induced miR-1a-3p expression, reducing cell death |
Mouse ischemia/reperfusion | Hearts of mice that underwent the I/R injury and treated with metformin | ||
[273] | Mouse ischemia/reperfusion | Hearts of mice that underwent the I/R injury and treated with metformin | Metformin reduced I/R induced-miR-34a-5p expression |
H9C2 rat cardiomyocyte cells | Oxygen-glucose deprivation/recovery and treatment with metformin | Metformin reduced miR-34a-5p levels through decreasing SIRT1-p53 activity | |
90 ACS (STEMI) patients | Metformin 3-months treatment pre-infarction | Metformin reduced serum miR-34a levels and CKMB activity and mitigated PCI-induced reperfusion injury | |
Thoracic aortas of diabetic rats | Liraglutide treatment | Liraglutide reduced miR-34a-5p and increased the anti-apoptotic protein Bcl2 and SIRT1, contrasting cell death | |
[280] | 25 patients with T2DM | Serum from patients with DM treated with liraglutide | Liraglutide induced the expression of miR-130a-3p, miR-27b-3p, and miR-210-3p |
[338] | Mouse MCAO | Brain after MCAO and metformin treatment | Metformin reduced H19-induced oxidative stress injury |
[282] | 10 frail old adults with HFpEF and DM | Whole blood after 3 months-treatment with empagliflozin or metformin or insulin | Empagliflozin specifically reduced miR-21 and miR-92 levels compared to metformin- or insulin-treated HFpEF patients and to controls |
Anti-inflammatory/anti-aggregation drugs and non-coding RNAs. | |||
Reference | Study Population/experimental system | Treatment | Main findings |
[339] | 46 ischemic stroke patients | PBMNCs from stroke patients treated with ASA for 10 days | ASA induced miR-145-5p levels in stroke patients |
VSMCs | Cells treated with ASA | ASA increased miR-145-5p and decreased CD40 levels, respectively, reducing VSMCs proliferation | |
[340] | Platelets of 12 ASA -treated CVD patients (6 with low and 6 high platelet reactivity) | ASA treatment | miR-135a-5p and miR-204-5p levels correlated with platelet reactivity |
[341] | Platelets of 945 acute coronary syndrome patients | ASA treatment | -Lower miR-19b‐1‐5p expression was associated to ASA insensitivity and to a higher risk of MACCE - Low miR-223 was a predictor of responsiveness to antiplatelet therapies |