Key result
Endothelial SIRT3 deficiency impairs glycolysis and increases ROS to promote coronary microvascular dysfunction and HFpEF.
Why the study?
Coronary microvascular dysfunction contributes to HFpEF, but the role of SIRT3-mediated endothelial metabolic reprogramming in this process requires summarization.
Impairment of SIRT3-mediated endothelial cell metabolism may contribute to coronary microvascular dysfunction and the development of heart failure with preserved ejection fraction.
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SIRT3 modulation in endothelial cells merits targeted study in HFpEF; hypothesis-generating and should not yet alter practice.
Zeng et al. (2019) conducted a review in Heart failure with preserved ejection fraction (HFpEF). SIRT3 was evaluated. SIRT3 deficiency in endothelial cells impairs glycolysis, increases reactive oxygen species, and disrupts cell communication, promoting coronary microvascular dysfunction and HFpEF.
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