Key result
Higher ApoM is linked to lower mortality in anthracycline-induced heart failure by sustaining myocardial autophagic flux.
Why the study?
Apolipoprotein M binds sphingosine-1-phosphate and is inversely associated with mortality in human heart failure, but its role in anthracycline cardiotoxicity was unclear.
Does Apolipoprotein M attenuate anthracycline cardiotoxicity and mortality in mice and humans?
Does Apolipoprotein M attenuate anthracycline cardiotoxicity and mortality in mice and humans?
Apolipoprotein M protects against anthracycline-induced cardiotoxicity and is inversely associated with mortality in patients with anthracycline-induced heart failure.
Hypothesis-generating for apolipoprotein M in anthracycline cardiotoxicity; leaves open translation to human therapy.
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.
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Guo et al. (2023) studied Anthracycline-induced heart failure. Apolipoprotein M (ApoM) was evaluated on Mortality and cardiotoxicity. Apolipoprotein M is inversely associated with mortality in patients with anthracycline-induced heart failure and attenuates doxorubicin cardiotoxicity by sustaining myocardial autophagic flux.
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