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Autophagy-mediated metabolic effects of aspirin

Castoldi, Francesca, Humeau, Juliette, Martins, Isabelle, Lachkar, Sylvie, Loew, Damarys, Dingli, Florent, Durand, Sylvère, Enot, David, Bossut, Noëlie, Chery, Alexis, Aprahamian, Fanny, Demont, Yohann, Opolon, Paule, Signolle, Nicolas, Sauvat, Allan, Semeraro, Michaela, Bezu, Lucillia, Baracco, Elisa Elena, Vacchelli, Erika, Pol, Jonathan G., Lévesque, Sarah, Bloy, Norma, Sica, Valentina, Maiuri, Maria Chiara, Kroemer, Guido, Pietrocola, Federico·2020·Cell Death Discovery
DOI 10.1038/s41420-020-00365-0PMC PMC7687910
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Abstract

Salicylate, the active derivative of aspirin (acetylsalicylate), recapitulates the mode of action of caloric restriction inasmuch as it stimulates autophagy through the inhibition of the acetyltransferase activity of EP300. Here, we directly compared the metabolic effects of aspirin medication with those elicited by 48 h fasting in mice, revealing convergent alterations in the plasma and the heart metabolome. Aspirin caused a transient reduction of general protein acetylation in blood leukocytes, accompanied by the induction of autophagy. However, these effects on global protein acetylation could not be attributed to the mere inhibition of EP300, as determined by epistatic experiments and exploration of the acetyl-proteome from salicylate-treated EP300-deficient cells. Aspirin reduced high-fat diet-induced obesity, diabetes, and hepatosteatosis. These aspirin effects were observed in autophagy-competent mice but not in two different models of genetic (Atg4b−/− or Bcln1+/−) autophagy-deficiency. Aspirin also improved tumor control by immunogenic chemotherapeutics, and this effect was lost in T cell-deficient mice, as well as upon knockdown of an essential autophagy gene (Atg5) in cancer cells. Hence, the health-improving effects of aspirin depend on autophagy.

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Crossref · 10.1038/s41420-020-00365-0

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  • EP300 is the target of the longevity-enhancing drugs nordihydroguairaretic acid and salicylate.

    “Among these factors, EP300 is the target of the longevity-enhancing drugs nordihydroguairaretic acid 118 and salicylate 119 .”

    From Hallmarks of aging: An expanding universe (2023) · cites this paper as [119]

    The Introduction states that salicylate inhibits EP300, supporting the part of the sentence to which this citation is attached. It discusses possible effects on age-related disease but does not establish that salicylate enhances longevity. The separate claim about nordihydroguaiaretic acid is attached to citation 118, not this source. (LLM, conf=0.84)

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Research works printed but not linked: 43

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Metadata

Authors
Castoldi, F., Humeau, J., Martins, I., Lachkar, S., Loew, D., Dingli, F., Durand, S., Enot, D., Bossut, N., Chery, A., Aprahamian, F., Demont, Y., Opolon, P., Signolle, N., Sauvat, A., Semeraro, M., Bezu, L., Baracco, E. E., Vacchelli, E., Pol, J. G., Lévesque, S., Bloy, N., Sica, V., Maiuri, M. C., Kroemer, G., & Pietrocola, F.
ORCID
Venue
Cell Death Discovery
Publisher
Springer Science and Business Media LLC
Published
2020-11-24
Volume
6
Issue
1
ISSN
2058-7716
DOI
10.1038/s41420-020-00365-0
PMC
PMC7687910
Cited by
27
References
7
Language
en
Licence

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