Key result
EPA, but not DHA, prevented fibrosis following transverse aortic constriction, though neither prevented contractile dysfunction.
Why the study?
Does EPA or DHA prevent fibrosis and contractile dysfunction in a pressure overload-induced heart failure model?
Does EPA or DHA prevent fibrosis and contractile dysfunction in a pressure overload-induced heart failure model?
EPA, but not DHA, prevents cardiac fibrosis in a pressure overload model, potentially via FFA receptor 4, suggesting a novel therapeutic avenue for HFpEF.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for EPA-specific antifibrosis in pressure overload; prospective human trials needed before clinical consideration.
Heart failure with preserved ejection fraction (HFpEF) is half of all HF, but standard HF therapies are ineffective. Diastolic dysfunction, often secondary to interstitial fibrosis, is common in HFpEF. Previously, we found that supra-physiologic levels of ω3-PUFAs produced by 12 weeks of ω3-dietary supplementation prevented fibrosis and contractile dysfunction following pressure overload [transverse aortic constriction (TAC)], a model that resembles aspects of remodeling in HFpEF. This raised several questions regarding ω3-concentration-dependent cardioprotection, the specific role of EPA and DHA, and the relationship between prevention of fibrosis and contractile dysfunction. To achieve more clinically relevant ω3-levels and test individual ω3-PUFAs, we shortened the ω3-diet regimen and used EPA- and DHA-specific diets to examine remodeling following TAC. The shorter diet regimen produced ω3-PUFA levels closer to Western clinics. Further, EPA, but not DHA, prevented fibrosis following TAC. However, neither ω3-PUFA prevented contractile dysfunction, perhaps due to reduced uptake of ω3-PUFA. Interestingly, EPA did not accumulate in cardiac fibroblasts. However, FFA receptor 4, a G protein-coupled receptor for ω3-PUFAs, was sufficient and required to block transforming growth factor β1-fibrotic signaling in cultured cardiac fibroblasts, suggesting a novel mechanism for EPA. In summary, EPA-mediated prevention of fibrosis could represent a novel therapy for HFpEF.
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Eclov et al. (2015) studied Heart failure with preserved ejection fraction (HFpEF). EPA-specific diet vs. DHA-specific diet was evaluated on Fibrosis and contractile dysfunction following transverse aortic constriction (TAC). EPA, but not DHA, prevented fibrosis following transverse aortic constriction, though neither prevented contractile dysfunction.
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