Communications Biology (Mar 2023)
The SGLT2 inhibitor empagliflozin improves cardiac energy status via mitochondrial ATP production in diabetic mice
- Jungmi Choi,
- Naoki Matoba,
- Daiki Setoyama,
- Daiki Watanabe,
- Yuichiro Ohnishi,
- Ryuto Yasui,
- Yuichirou Kitai,
- Aki Oomachi,
- Yutaro Kotobuki,
- Yoichi Nishiya,
- Michael Paul Pieper,
- Hiromi Imamura,
- Motoko Yanagita,
- Masamichi Yamamoto
Affiliations
- Jungmi Choi
- Department of Research Promotion and Management, National Cerebral and Cardiovascular Center
- Naoki Matoba
- Department of Research Promotion and Management, National Cerebral and Cardiovascular Center
- Daiki Setoyama
- Department of Clinical Chemistry and Laboratory Medicine, Kyushu University Hospital
- Daiki Watanabe
- Department of Research Promotion and Management, National Cerebral and Cardiovascular Center
- Yuichiro Ohnishi
- Department of Research Promotion and Management, National Cerebral and Cardiovascular Center
- Ryuto Yasui
- Department of Research Promotion and Management, National Cerebral and Cardiovascular Center
- Yuichirou Kitai
- Department of Nephrology, Kyoto University Graduate School of Medicine, Kyoto University
- Aki Oomachi
- Department of Research Promotion and Management, National Cerebral and Cardiovascular Center
- Yutaro Kotobuki
- Medicine Division, Nippon Boehringer Ingelheim Co., Ltd.
- Yoichi Nishiya
- Medicine Division, Nippon Boehringer Ingelheim Co., Ltd.
- Michael Paul Pieper
- CardioMetabolic Diseases Research, Boehringer Ingelheim Pharma GmbH & Co. KG
- Hiromi Imamura
- Department of Functional Biology, Graduate School of Biostudies, Kyoto University
- Motoko Yanagita
- Department of Nephrology, Kyoto University Graduate School of Medicine, Kyoto University
- Masamichi Yamamoto
- Department of Research Promotion and Management, National Cerebral and Cardiovascular Center
- DOI
- https://doi.org/10.1038/s42003-023-04663-y
- Journal volume & issue
-
Vol. 6,
no. 1
pp. 1 – 9
Abstract
The SGLT2 inhibitor, Empagliflozin, is shown to exert cardioprotective effects by increasing mitochondrial ATP in a mouse model of diabetes.
