Myocardial ketone body oxidation contributes to empagliflozin-induced improvements in cardiac contractility in murine heart failure.

• Tác giả: Anna M Feringa, Belend Mahmoud, Kirsten T Nijholt, Constantin Laurent Palm, Pablo I Sanchez-Aguilera, Huitzilihuitl Saucedo-Orozco, Elisabeth Marloes Schouten, Herman H W Silljé, Peter van der Meer, Suzanne Nathalie Voorrips, B Daan Westenbrink, Salva R Yurista
• Ngôn ngữ: eng
• Ký hiệu phân loại: 616.129 *Heart failure
• Thông tin xuất bản: England : European journal of heart failure , 2025
• Bộ sưu tập: NCBI
• ID: 696267

Tóm tắt

AIMS: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) improve cardiac performance and clinical outcomes in patients with heart failure, yet mechanisms underlying these beneficial effects remain incompletely understood. We sought to determine whether SGLT2i-induced improvements in cardiac function are dependent on increased cardiac oxidation of ketone bodies. METHODS AND RESULTS: We employed a mouse model with a cardiac-specific knock-out of the enzyme D-β-hydroxybutyrate dehydrogenase-1 (BDH1 CONCLUSION: The beneficial effects of empagliflozin on cardiac contractility in post-MI heart failure are attenuated in mice which are incapable of oxidizing the ketone body β-hydroxybutyrate in their hearts. These findings suggest that enhanced cardiac ketone body oxidation contributes to the cardioprotective effects of SGLT2i.