School of Rehabilitation, Capital Medical University, Beijing, China.
Department of Spinal and Neural Functional Reconstruction, China Rehabilitation Research Center, Beijing, China.
Front Immunol. 2024 Mar 13;15:1368203. doi: 10.3389/fimmu.2024.1368203. eCollection 2024.
Spinal cord injury (SCI) results in a large amount of tissue cell debris in the lesion site, which interacts with various cytokines, including inflammatory factors, and the intrinsic glial environment of the central nervous system (CNS) to form an inhibitory microenvironment that impedes nerve regeneration. The efficient clearance of tissue debris is crucial for the resolution of the inhibitory microenvironment after SCI. Macrophages are the main cells responsible for tissue debris removal after SCI. However, the high lipid content in tissue debris and the dysregulation of lipid metabolism within macrophages lead to their transformation into foamy macrophages during the phagocytic process. This phenotypic shift is associated with a further pro-inflammatory polarization that may aggravate neurological deterioration and hamper nerve repair. In this review, we summarize the phenotype and metabolism of macrophages under inflammatory conditions, as well as the mechanisms and consequences of foam cell formation after SCI. Moreover, we discuss two strategies for foam cell modulation and several potential therapeutic targets that may enhance the treatment of SCI.
脊髓损伤（SCI）会在损伤部位产生大量的组织细胞碎片，这些碎片与各种细胞因子（包括炎症因子）相互作用，并与中枢神经系统（CNS）的固有神经胶质环境相互作用，形成抑制性微环境，阻碍神经再生。有效地清除组织碎片对于 SCI 后抑制性微环境的解决至关重要。巨噬细胞是 SCI 后负责清除组织碎片的主要细胞。然而，组织碎片中的高脂质含量和巨噬细胞内脂质代谢的失调导致它们在吞噬过程中转化为泡沫巨噬细胞。这种表型转变与进一步的促炎极化有关，可能会加重神经恶化并阻碍神经修复。在这篇综述中，我们总结了炎症条件下巨噬细胞的表型和代谢，以及 SCI 后泡沫细胞形成的机制和后果。此外，我们讨论了两种泡沫细胞调节策略和几个可能增强 SCI 治疗效果的潜在治疗靶点。
