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Reversible ALKBH5 cytosolic aggregation accelerates cellular senescence.

Liqian Chen1,2,3, Zixin Chen1, Jiahui Mo1,4

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|August 15, 2025
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Cellular senescence, a hallmark of aging, is promoted by the cytoplasmic aggregation of ALKBH5, an m6A demethylase. Restoring ALKBH5 nuclear entry via m6A RNA or NLS-ALKBH5 alleviates senescence.

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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Aging Research

Background:

  • Cellular senescence is a key factor in aging and age-related diseases.
  • The precise role of ALKBH5, an m6A demethylase, in cellular senescence is not fully understood.

Purpose of the Study:

  • To elucidate the mechanism by which ALKBH5 influences cellular senescence.
  • To identify potential therapeutic strategies targeting ALKBH5 for aging and age-related diseases.

Main Methods:

  • Investigated the aggregation of ALKBH5 in the cytoplasm and its effect on m6A modification.
  • Examined the interaction between ALKBH5, Nucleoporin p62 (Nup62), and nuclear translocation.
  • Utilized m6A-labeled RNA administration and NLS-ALKBH5 to modulate ALKBH5 localization and senescence.

Main Results:

  • ALKBH5 cytoplasmic aggregation promotes cellular senescence by causing cytosolic retention and m6A dysregulation of Cdk2 RNA.
  • ALKBH5 aggregation creates a feedback loop that exacerbates m6A imbalance.
  • ALKBH5 nuclear translocation depends on binding Nup62; aggregation traps ALKBH5 and Nup62 in the cytoplasm, inhibiting nuclear entry and inducing senescence.

Conclusions:

  • ALKBH5 aggregation in the cytoplasm is a novel mechanism driving cellular senescence.
  • Targeting ALKBH5 aggregation and restoring its nuclear entry presents a promising therapeutic strategy for aging and age-related diseases.