Key result
Mineralocorticoid receptor antagonist exposure was associated with lower epicardial fat levels of the fatty acid transporter CD36 and higher intelectin-1 expression.
Why the study?
Epicardial fat thickness is associated with cardiovascular disease and MRAs affect adipose tissue, prompting analysis of main epicardial fat genesis and inflammation cell markers and their regulation by risk factors and MRA.
Does mineralocorticoid receptor antagonist exposure modulate the expression of fatty acid transporters and anti-inflammatory markers in the epicardial fat of patients with cardiovascular disease?
Observational (n=137)
No
Does mineralocorticoid receptor antagonist exposure modulate the expression of fatty acid transporters and anti-inflammatory markers in the epicardial fat of patients with cardiovascular disease?
MRA exposure may favorably modulate epicardial adipose tissue remodeling by reducing fatty acid transporter expression and upregulating anti-inflammatory pathways like ITLN-1.
Answers are grounded in this paper and cite their sources.
MRA-associated epicardial fat changes should not change practice; leaves open causal effects on adipose remodeling in heart failure.
Epicardial fat thickness is associated with cardiovascular disease. Mineralocorticoid receptor antagonist (MRA), a pharmaceutical treatment for CVD, was found to have an effect on adipose tissue. Our aim was to analyse the main epicardial fat genesis and inflammation-involved cell markers and their regulation by risk factors and MRA. We included blood and epicardial or subcutaneous fat (EAT or SAT) from 71 patients undergoing heart surgery and blood from 66 patients with heart failure. Cell types (transcripts or proteins) were analysed by real-time polymerase chain reaction or immunohistochemistry. Plasma proteins were analysed by Luminex technology or enzyme-linked immunoassay. Our results showed an upregulation of fatty acid transporter levels after aldosterone-induced genesis. The MRA intake was the main factor associated with lower levels in epicardial fat. On the contrary, MRA upregulated the levels and its secretion of the anti-inflammatory marker intelectin 1 and reduced the proliferation of epicardial fibroblasts. Our results have shown the local MRA intake effect on fatty acid transporters and anti-inflammatory marker levels and the proliferation rate on epicardial fat fibroblasts. They suggest the role of MRA on epicardial fat genesis and remodelling in patients with cardiovascular disease. Translational perspective: the knowledge of epicardial fat genesis and its modulation by drugs might be useful for improving the treatments of cardiovascular disease.
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Fu et al. (2022) conducted an observational in Cardiovascular disease and heart failure (n=137). Mineralocorticoid receptor antagonist (MRA) vs. No MRA intake was evaluated on Epicardial fat CD36 expression level (a.u.) (β = -0.042, p=<0.01). Mineralocorticoid receptor antagonist exposure was associated with lower epicardial fat levels of the fatty acid transporter CD36 and higher intelectin-1 expression.
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