Cardioprotective mechanism of ω-3 fatty acid icosapent ethyl (IPE) in cardiomyocytes: role in high glucose and shear stress-induced mechano-transduction dysregulation
Authors' conclusion
Our results demonstrate a cardioprotective role of IPE through modulation of hyperglycaemia-induced mechano-transduction dysregulation, inflammation, and oxidative stress. Additionally, our results on a shear stress model showing that IPE restores upstream regulators of YAP/TAZ and reduces disturbed flow-induced activation of pro-inflammatory pathways, suggest that IPE may exert a therapeutic effect on cardiovascular disorders associated with disturbed blood flow and hemodynamic stress.
Study context
- Population
- Cardiomyocyte AC16 cells; patients with CVD and cardiometabolic diseases (meta-analyses)
- Comparison
- IPE vs no IPE under normal glucose (NG) or high glucose (HG) and shear stress; omega-3 in patients (meta-analyses)
- Outcome
- Meta-analyses of omega-3 in patients with cardiovascular and cardiometabolic diseases: LVEF% and inflammatory markers; IPE effects on YAP/TAZ activation and HG-induced inflammation, oxidative stress, metabolism and apoptosis markers in AC16 cardiomyocytes
Methodological detailsin vitro AC16 cardiomyocytes, dynamic flow (shear stress) model, meta-analyses of in vivo studies
- In vitro AC16 cardiomyocytes
- Dynamic flow (shear stress) model
- Meta-analyses of in vivo studies
Main finding
As reported in the abstract
Increase of LVEF% with omega-3
0.5
mean; 95% CI 0.1–0.9
Reduction of inflammatory markers with omega-3 (mean; 95% CI as printed: 2.05-0.44)
- 1.24
Original publication
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