Why the study?
The effect of endothelial microvesicles from obese/hypertensive adults on mediators of cardiomyocyte hypertrophy, fibrosis, and endothelial nitric oxide synthase expression had not been determined.
Do endothelial microvesicles from obese/hypertensive adults increase hypertrophic and fibrotic mediators in cardiomyocytes compared to those from normal weight/normotensive adults?
Do endothelial microvesicles from obese/hypertensive adults increase hypertrophic and fibrotic mediators in cardiomyocytes compared to those from normal weight/normotensive adults?
Endothelial microvesicles from obese/hypertensive adults may mediate the increased risk of cardiomyopathy and heart failure by promoting cardiomyocyte hypertrophy and fibrosis.
These in vitro effects merit in vivo validation; leaves open clinical translation in obese hypertension.
In the present study we determined the effect of endothelial microvesicles (EMVs) isolated from obese/hypertensive adults on mediators of cardiomyocyte hypertrophy [cardiac troponin T (cTnT), α-actinin, nuclear factor-kB (NF-kB)] and fibrosis [transforming growth factor (TGF-β), collagen1-α1] as well as endothelial nitric oxide synthase (eNOS) expression and NO production. EMVs from obese/hypertensive induced significantly higher expression of hypertrophic (cTnT, α-actinin, NF-kB) and fibrotic (TGF-β) proteins as well as significantly lower eNOS activation and NO production in cardiomyocytes than EMVs from normal weight/normotensive adults. EMVs are a potential mediating factor in the increased risk of cardiomyopathy and heart failure with obesity/hypertension.
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Fandl et al. (2023) studied this question.
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