Journal
AUTOPHAGY
Volume 16, Issue 1, Pages 181-182Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2019.1687967
Keywords
Aging; autophagy; B cells; EIF5A; hypusine; spermidine; TFEB; translation
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Funding
- Wellcome Trust Investigator Award [103830/Z/14/Z]
- China Scholarship Council-Nuffield Department of Medicine Scholarship
- Oxford-Elysium Prize Fellowship
- Wellcome Trust [103830/Z/14/Z] Funding Source: Wellcome Trust
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Organismal aging is associated with compromised cellular function, which can be partially attributed to accumulation of cellular damage. Being the major, if not only, cellular bulk-degradation mechanism, macroautophagy (hereafter autophagy) declines with age in multiple tissues and organisms. Spermidine is an endogenous polyamine metabolite that also declines with age. It prolongs lifespan and improves tissue functions of model organisms in an autophagy-dependent manner. We report that autophagic flux is significantly reduced in B cells from old mice. Spermidine induces autophagy and improves the function of both old mouse and old human B cells. Mechanistically, spermidine post-translationally modifies (hypusinates) the translation factor EIF5A. Hypusinated EIF5A specifically regulates the synthesis of the master autophagy and lysosome transcription factor, TFEB (transcription factor EB). This pathway declines with age in both mice and humans, which may eventually lead to declining autophagy and impaired tissue functions in old individuals.
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