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Updated: May 12, 2026

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DNMT3A dysfunction promotes neuroinflammation and exacerbates acute ischemic stroke.

Tian-Jie Lyu1,2, Xin Qiu1,2, Yubo Wang1,2

  • 1Department of Neurology Beijing Tiantan Hospital Capital Medical University Beijing China.

Medcomm
|July 15, 2024
PubMed
Summary

Somatic mutations in the DNMT3A gene, linked to clonal hematopoiesis (CHIP), worsen outcomes in acute ischemic stroke (AIS) patients. DNMT3A inhibition in mice increased stroke severity, suggesting a role in neuroinflammation and tissue damage.

Keywords:
DNMT3ARG108clonal hematopoiesisfunctional outcomeproinflammatory

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Area of Science:

  • Neuroscience
  • Genetics
  • Cardiovascular Science

Background:

  • Clonal hematopoiesis of indeterminate potential (CHIP) is linked to stroke risk.
  • The role of DNMT3A mutations in CHIP on acute ischemic stroke (AIS) outcomes is unknown.

Purpose of the Study:

  • To investigate the association between DNMT3A-driven CHIP and neurological disability in AIS patients.
  • To explore the mechanistic role of DNMT3A in a mouse model of ischemic stroke.

Main Methods:

  • Analysis of 8524 AIS patients for DNMT3A mutations and neurological outcomes.
  • Utilized a transient middle cerebral artery occlusion (tMCAO) mouse model.

Main Results:

  • DNMT3A-driven CHIP correlated with increased neurological disability in AIS patients.
  • DNMT3A inhibition in tMCAO mice amplified neutrophil proliferation and brain infiltration.
  • DNMT3A inhibition worsened infarct volume and neurobehavioral function in male mice.

Conclusions:

  • DNMT3A somatic mutations are linked to poorer neurological outcomes in AIS.
  • Potential mechanisms involve increased neutrophil activity and neuroinflammation.
  • Further research is warranted to understand DNMT3A's role in stroke pathophysiology.