Key result
Endogenous EETs emerge as potential HFpEF targets by inhibiting inflammation, fibrosis, and cardiac remodeling.
Why the study?
Effective therapy for HFpEF is lacking due to limited knowledge of its mechanism, prompting the exploration of novel endogenous protective therapeutics such as epoxyeicosatrienoic acids.
Do Epoxyeicosatrienoic acids (EETs) have therapeutic potential for alleviating the pathophysiology underlying heart failure with preserved ejection fraction (HFpEF)?
Do Epoxyeicosatrienoic acids (EETs) have therapeutic potential for alleviating the pathophysiology underlying heart failure with preserved ejection fraction (HFpEF)?
This review highlights the potential of Epoxyeicosatrienoic acids (EETs) as a novel therapeutic target for HFpEF due to their endogenous cardioprotective properties.
Heart failure with preserved ejection fraction (HFpEF) reduces the quality of life, costs substantial medical resources, and has a high mortality. However, we lack an effective therapy for HFpEF due to our limited knowledge of its mechanism. Therefore, it is crucial to explore novel therapeutics, such as those with endogenous protective roles, and seek new targeted therapies. Epoxyeicosatrienoic acids (EETs) are endogenous bioactive metabolites of arachidonic acids produced by cytochrome P450 (CYP) epoxygenases. EETs can function as endogenous cardioprotective factors with potent inhibitory roles in inflammation, endothelial dysfunction, cardiac remodeling, and fibrosis, which are the fundamental mechanisms of HFpEF. This suggests that EETs have the potential function to protect against HFpEF. Therefore, we present an overview of the ever-expanding world of EETs and how they might help alleviate the pathophysiology underlying HFpEF to provide new insights for research in this field.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2022) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Epoxyeicosatrienoic acids (EETs) was evaluated. Epoxyeicosatrienoic acids (EETs) function as endogenous cardioprotective factors that inhibit inflammation, endothelial dysfunction, cardiac remodeling, and fibrosis, suggesting potential as a therapeutic target for HFpEF.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: