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<p>Cerebral cavernous malformation (CCM) is a condition affecting the brain vasculature, characterized by endothelial dysfunction and abnormal vascular structure. In recent years, the gut-brain axis has emerged as a significant regulatory factor influencing cerebrovascular health. The gut microbiota, through its metabolites, immune modulation, and signaling interactions with the brain, plays a critical role in the pathogenesis of CCM. Research indicates that dysbiosis can trigger systemic inflammatory responses via pathways such as lipopolysaccharide (LPS) -TLR4, short-chain fatty acids (SCFAs), and trimethylamine N-oxide (TMAO), ultimately affecting cerebrovascular function and the integrity of the blood-brain barrier. Additionally, the gut-brain axis may influence the proliferation, migration, and apoptosis of endothelial cells, potentially promoting or inhibiting the development of CCM. Although the exact mechanisms linking the gut-brain axis and CCM remain unclear, existing studies suggest a potential key role in the pathological progression of CCM. This review explores the mechanisms by which the gut-brain axis contributes to CCM and proposes that targeting relevant pathways within the gut-brain axis may offer new therapeutic strategies for CCM.</p>

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MEKK3 bridges gut-brain communication and cerebral cavernous malformation pathogenesis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月27日

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  • Peng Cheng,
  • Hongkuan Han,
  • Ying Huang,
  • Yang Shen,
  • Xuan Jiang,
  • Xiaoxiong Song,
  • Cheng Qian,
  • Lei Chen,
  • Yang Zhao

摘要

Cerebral cavernous malformation (CCM) is a condition affecting the brain vasculature, characterized by endothelial dysfunction and abnormal vascular structure. In recent years, the gut-brain axis has emerged as a significant regulatory factor influencing cerebrovascular health. The gut microbiota, through its metabolites, immune modulation, and signaling interactions with the brain, plays a critical role in the pathogenesis of CCM. Research indicates that dysbiosis can trigger systemic inflammatory responses via pathways such as lipopolysaccharide (LPS) -TLR4, short-chain fatty acids (SCFAs), and trimethylamine N-oxide (TMAO), ultimately affecting cerebrovascular function and the integrity of the blood-brain barrier. Additionally, the gut-brain axis may influence the proliferation, migration, and apoptosis of endothelial cells, potentially promoting or inhibiting the development of CCM. Although the exact mechanisms linking the gut-brain axis and CCM remain unclear, existing studies suggest a potential key role in the pathological progression of CCM. This review explores the mechanisms by which the gut-brain axis contributes to CCM and proposes that targeting relevant pathways within the gut-brain axis may offer new therapeutic strategies for CCM.