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<p>Cerebral small vessel disease (CSVD) encompasses diffuse brain lesions arising from structural injury to small vessels, and is closely associated with chronic hypoperfusion and blood–brain barrier (BBB) dysfunction. Its insidious onset and heterogeneous clinical manifestations render elucidation of its pathogenesis and development of targeted interventions of paramount clinical importance. Transforming growth factorβ (TGFβ), a pivotal regulator of vascular homeostasis, exerts bidirectional effects within the neurovascular unit (NVU) during CSVD: under physiological conditions, TGFβ maintains barrier integrity by modulating endothelial tight junction proteins and pericyte adhesion; under pathological stress, dysregulated TGFβ signaling induces endothelial dysfunction, pericyte degeneration and neuroinflammation, thereby promoting white-matter injury. Precise, spatiotemporal modulation of TGFβ pathways therefore represents a promising avenue for stage-specific, molecularly targeted therapy in CSVD.</p>

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Role of transforming growth factorβ in neurovascular unit during cerebral small vessel disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月28日

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  • Yangjie Li,
  • Ying Cai,
  • Kangling Xie,
  • Fan Hu,
  • Jiaohao Li,
  • Cui Li,
  • Runjie Zhang,
  • Zhengwei Zhong

摘要

Cerebral small vessel disease (CSVD) encompasses diffuse brain lesions arising from structural injury to small vessels, and is closely associated with chronic hypoperfusion and blood–brain barrier (BBB) dysfunction. Its insidious onset and heterogeneous clinical manifestations render elucidation of its pathogenesis and development of targeted interventions of paramount clinical importance. Transforming growth factorβ (TGFβ), a pivotal regulator of vascular homeostasis, exerts bidirectional effects within the neurovascular unit (NVU) during CSVD: under physiological conditions, TGFβ maintains barrier integrity by modulating endothelial tight junction proteins and pericyte adhesion; under pathological stress, dysregulated TGFβ signaling induces endothelial dysfunction, pericyte degeneration and neuroinflammation, thereby promoting white-matter injury. Precise, spatiotemporal modulation of TGFβ pathways therefore represents a promising avenue for stage-specific, molecularly targeted therapy in CSVD.