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Liquid-liquid phase separation of RBM33 facilitates hippocampus aging by inducing microglial senescence by activating

Xiaowen Yang1, Lin Wei2, Saifeng Zhong3

  • 1Department of Clinical Laboratory, Taihe Hospital, The Affiliated Hospital of Hubei University of Medicine, Shiyan 442000, China; Department of Clinical Laboratory, Hunan Provincial People's Hospital, The First-Affiliated Hospital of Hunan Normal University/Department of Laboratory Medicine of School of Medicine, Hunan Normal University, Changsha 410000, China; Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China.

International Journal of Biological Macromolecules
|April 11, 2025
PubMed

Insights

RNA-binding protein 33 (RBM33) promotes brain aging by inducing microglial senescence, impairing hippocampus-dependent memory. Targeting the RBM33/p21 axis may combat cognitive decline and brain aging.

Area of Science:

  • Neuroscience
  • Aging Research
  • Molecular Biology

Background:

  • Microglia are crucial for hippocampus-dependent memory and cognitive function.
  • Microglial aging contributes to brain aging and neurodegenerative diseases, but mechanisms are unclear.
  • RNA-binding protein 33 (RBM33) is implicated in aging processes.

Purpose of the Study:

  • To investigate the role of RBM33 in hippocampal aging and cognitive decline.
  • To elucidate the molecular mechanisms by which RBM33 influences microglial senescence and brain aging.

Main Methods:

  • Analysis of RBM33 expression in aged mice and senescent microglia.
  • Genetic manipulation of RBM33 in the hippocampus (knockout and overexpression models).
  • Investigation of RBM33 liquid-liquid phase separation (LLPS) and its interaction with the CDKN1A (p21) promoter.

Main Results:

  • RBM33 expression is elevated in aged hippocampus and senescent microglia.
  • Hippocampal RBM33 deletion alleviates age-related memory deficits, while overexpression exacerbates them.
  • RBM33 LLPS drives microglial senescence via non-canonical regulation of the p21 promoter, impairing cognitive function.

Conclusions:

  • RBM33 acts as an age-promoting factor in the hippocampus by inducing microglial senescence.
  • The RBM33 LLPS/p21 axis is a key driver of brain aging and cognitive decline.
  • Targeting the RBM33 LLPS/p21 axis offers a potential therapeutic strategy for age-related cognitive impairment.
Keywords:
Hippocampus agingMicroglial senescenceRBM33

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