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Table 4 Anti-diabetic, anti-inflammatory/anti-aggregation drugs impacting on ncRNAs

From: Cardiovascular complications of diabetes: role of non-coding RNAs in the crosstalk between immune and cardiovascular systems

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

  1. ACS: acute coronary syndrome, ASA: acetylsalicylic acid, Bcl2: B-cell lymphoma 2, CKMB: creatine kinase MB, CVD: cardiovascular disease, DM: diabetes mellitus, ECs: endothelial cells HFpEF: heart failure with preserved ejection fraction, HG: high glucose, MCAO: middle cerebral artery occlusion, I/R: Ischemia-reperfusion, MACCE: major adverse cardiac and cerebrovascular events, PBMNCs: peripheral blood mononuclear cells, PCI: percutaneous coronary intervention, PTEN: phosphatase and tensin homolog, SIRT1: Silent information regulator 1, STEMI: ST-segment elevation myocardial infarction, VSMCs: vascular smooth muscle cells.