Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury
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Apolipoprotein M (ApoM) binds sphingosine-1-phosphate (S1P) and is inversely associated with mortality in human heart failure (HF). Here, we show that anthracyclines such as doxorubicin (Dox) reduce circulating ApoM in mice and humans, that ApoM is inversely associated with mortality in patients with anthracycline-induced heart failure, and ApoM heterozygosity in mice increases Dox-induced mortality. In the setting of Dox stress, our studies suggest ApoM can help sustain myocardial autophagic flux in a post-transcriptional manner, attenuate Dox cardiotoxicity, and prevent lysosomal injury.
Original language | English |
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Journal | JACC: Basic to Translational Science |
Volume | 8 |
Issue number | 3 |
Pages (from-to) | 340-355 |
ISSN | 2452-302X |
DOIs | |
Publication status | Published - 2023 |
Bibliographical note
Publisher Copyright:
© 2023 The Authors
- anthracycline, apolipoprotein M, autophagy, cardiomyopathy, TFEB
Research areas
ID: 340402091