Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury

Zhen Guo, Carla Valenzuela Ripoll, Antonino Picataggi, David Rawnsley, Mualla Ozcan, Julio A. Chirinos, Ezhilarasi Chendamarai, Amanda Girardi, Terrence Riehl, Hosannah Evie, Ahmed Diab, Attila Kovacs, Krzysztof Hyrc, Xiucui Ma, Aarti Asnani, Swapnil V. Shewale, Marielle Scherrer-Crosbie, Lauren Ashley Cowart, John S. Parks, Lei ZhaoDavid Gordon, Francisco Ramirez-Valle, Kenneth B. Margulies, Thomas P. Cappola, Ankit A. Desai, Lauren N. Pedersen, Carmen Bergom, Nathan Stitziel, Michael Rettig, John Dipersio, Stefan Hajny, Christina Christoffersen, Abhinav Diwan, Ali Javaheri

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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 languageEnglish
Pages (from-to)340-355
Number of pages16
JournalJACC: Basic to Translational Science
Issue number3
StatePublished - Mar 2023


  • TFEB
  • anthracycline
  • apolipoprotein M
  • autophagy
  • cardiomyopathy


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