Suppr超能文献

多发性硬化症病灶中的细胞外基质。

The extracellular matrix in multiple sclerosis lesions.

作者信息

Sobel R A

机构信息

Pathology and Laboratory Services, Veterans Administration Health Care System, Palo Alto, Calif 94304, USA.

出版信息

J Neuropathol Exp Neurol. 1998 Mar;57(3):205-17. doi: 10.1097/00005072-199803000-00001.

Abstract

Receptor-mediated recognition of extracellular matrix (ECM) molecules transduces intracellular signals that determine many cellular behaviors under normal and pathological conditions. This review briefly describes the major central nervous system (CNS) white matter ECM molecules and their receptors, the mechanisms by which the ECM may be altered in multiple sclerosis (MS) lesions, and potential roles for inflammatory and CNS resident cell interactions with specific ECM molecules in these lesions. In acute lesions, ECM recognition and cell signaling contribute to leukocyte migration through blood vessel walls, and within the CNS, through leukocyte and CNS resident cell immune activation and demyelination. An abnormal ECM in chronic MS lesions may preclude ECM-dependent developmental processes that lead to remyelination and axon regeneration. Thus, the composition of the ECM and the cellular recognition of its individual components may be critical to the pathogenesis of all stages of MS. An understanding of these complex interactions may lead to additional strategies for intervention and the promotion of reparative processes in MS patients.

摘要

受体介导的细胞外基质(ECM)分子识别可转导细胞内信号,这些信号决定了正常和病理条件下的许多细胞行为。本综述简要描述了主要的中枢神经系统(CNS)白质ECM分子及其受体、ECM在多发性硬化症(MS)病变中可能发生改变的机制,以及炎症细胞与中枢神经系统驻留细胞与这些病变中特定ECM分子相互作用的潜在作用。在急性病变中,ECM识别和细胞信号传导有助于白细胞穿过血管壁迁移,并在中枢神经系统内通过白细胞和中枢神经系统驻留细胞的免疫激活和脱髓鞘作用。慢性MS病变中的异常ECM可能会妨碍依赖ECM的发育过程,而这些过程会导致髓鞘再生和轴突再生。因此,ECM的组成及其各个成分的细胞识别可能对MS各个阶段的发病机制至关重要。了解这些复杂的相互作用可能会为MS患者带来额外的干预策略和促进修复过程的方法。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验