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Editorial
. 2025 Feb;7(2):185-187.
doi: 10.1016/j.jaccao.2025.01.005.

Empagliflozin to Prevent Doxorubicin Cardiotoxicity

Affiliations
Editorial

Empagliflozin to Prevent Doxorubicin Cardiotoxicity

Zhen Guo et al. JACC CardioOncol. 2025 Feb.
No abstract available

Keywords: anthracycline; cardio-oncology; cardiomyopathy; cardioprotection; doxorubicin cardiotoxicity; heart failure; imaging; ketosis; metabolism; myocardial energetics; pigs; sodium-glucose contransporter-2 inhibitors; treatment.

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Conflict of interest statement

Funding Support and Author Disclosures Dr Javaheri was supported by the National Heart, Lung, and Blood Institute (grants K08HL138262 and 1R01HL155344), the Children’s Discovery Institute of Washington University and St. Louis Children’s Hospital (grant MC-FR-2020-919), the Diabetes Research Center at Washington University in St. Louis of the National Institutes of Health (grant P30DK020579), the Nutrition Obesity Research Center of the National Institutes of Health (grant P30DK056341), and the Longer Life Foundation. Dr Guo was supported by the American Heart Association Second Century Early Faculty Independence Award (grant 24SCEFIA125647), an American Heart Association Postdoctoral Fellowship Award (898679), and the Division of Cardiology at Washington University (grant GF0012995). Dr Javaheri has a pending patent for fusion protein nanodiscs for the treatment of patients with HF and eye disease; is a member of the scientific advisory board of Mobius Scientific; and has received research funding from AstraZeneca and Bitterroot Bio, unrelated to the studies discussed in this paper. Dr Guo has reported that he has no relationships relevant to the contents of this paper to disclose.

Figures

None
Graphical abstract
Figure 1
Figure 1
Nutrient Hypothesis of SGLT2i Action in the Myocardium The schematic depicts 2 different hypotheses regarding sodium-glucose cotransporter-2 inhibitor (SGLT2i) therapy. (Left) SGLT2i therapy either directly or indirectly mimics nutrient deprivation, with AMP-activated protein kinase (AMPK) phosphorylation and sirtuin-1 (SIRT1) deacetylation (D-Ac), leading to transcription factor EB (TFEB) activation, which would promote cardiomyocyte atrophy contributing to reduced left ventricular (LV) mass. (Right) In contrast, under nutrient-rich conditions, mammalian target of rapamycin (mTOR) and protein kinase B (AKT) phosphorylation leads to TFEB phosphorylation and cytoplasmic sequestration, preventing cardiomyocyte atrophy. P = phosphorylation.

Comment on

References

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