Yu Haihan, Zhang Li, Song Bo, Ren Kaidi, Chen Xing, Dai Yuwan, Yang Yang, Xu Yuming, Wei Ziqing
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P. R. China.
Key Clinical Laboratory of Henan Province, Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P. R. China.
J Transl Med. 2025 Jul 11;23(1):782. doi: 10.1186/s12967-025-06799-3.
Ischemic stroke, the most prevalent type of stroke globally, poses significant challenges due to its high incidence, morbidity, and long-term disability. Microglia, the resident immune cells of the central nervous system (CNS), play a dual role in the context of ischemic stroke. While they contribute to neuroinflammation by releasing pro-inflammatory cytokines and exacerbating neuronal injury, they also facilitate tissue repair, angiogenesis, and restoration of the blood-brain barrier (BBB) integrity through the secretion of anti-inflammatory and neurotrophic factors. Triggering receptor expressed on myeloid cells 2 (TREM2), predominantly expressed on microglia, is a critical regulator of microglial proliferation, survival, phagocytosis, polarization, inflammation, and metabolism. TREM2 has emerged as a key modulator of immune responses in ischemic stroke. This review provides a comprehensive examination of the multifaceted roles of TREM2 in microglial biology during ischemic stroke, integrating current insights into its molecular mechanisms. Furthermore, it highlights TREM2's potential as a transformative therapeutic target, advancing our understanding of neuroimmune regulation and promoting recovery after stroke.
缺血性中风是全球最常见的中风类型，因其高发病率、高致残率和长期残疾而带来重大挑战。小胶质细胞是中枢神经系统（CNS）的常驻免疫细胞，在缺血性中风的情况下发挥双重作用。虽然它们通过释放促炎细胞因子导致神经炎症并加剧神经元损伤，但它们也通过分泌抗炎和神经营养因子促进组织修复、血管生成和血脑屏障（BBB）完整性的恢复。髓系细胞触发受体2（TREM2）主要在小胶质细胞上表达，是小胶质细胞增殖、存活、吞噬作用、极化、炎症和代谢的关键调节因子。TREM2已成为缺血性中风免疫反应的关键调节因子。本综述全面探讨了TREM2在缺血性中风期间小胶质细胞生物学中的多方面作用，整合了当前对其分子机制的见解。此外，它强调了TREM2作为一种变革性治疗靶点的潜力，增进了我们对神经免疫调节的理解，并促进中风后的恢复。
