Arthritis Center, Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Rome, Italy.
Immunol Res. 2018 Dec;66(6):655-662. doi: 10.1007/s12026-018-9053-0.
Microparticles (MPs) are small membrane vesicles released by many cell types under physiological and pathological conditions. In the last years, these particles were considered as inert cell debris, but recently many studies have demonstrated they could have a role in intercellular communication. Increased levels of MPs have been reported in various pathological conditions including infections, malignancies, and autoimmune diseases, such as rheumatoid arthritis (RA). RA is an autoimmune systemic inflammatory disease characterized by chronic synovial inflammation, resulting in cartilage and bone damage with accelerated atherosclerosis increasing mortality. According to the literature data, also MPs could have a role in endothelial dysfunction, contributing to atherosclerosis in RA patients. Moreover many researchers have shown that a dysregulated autophagy seems to be involved in endothelial dysfunction. Autophagy is a reparative process by which cytoplasmic components are sequestered in double-membrane vesicles and degraded on fusion with lysosomal compartments. It has been shown in many works that basal autophagy is essential to proper vascular function. Taking into account these considerations, we hypothesized that in RA patients MPs could contribute to atherosclerosis process by dysregulation of endothelial autophagy process.
微粒（MPs）是许多细胞类型在生理和病理条件下释放的小膜囊泡。在过去的几年中，这些颗粒被认为是惰性的细胞碎片，但最近的许多研究表明它们可能在细胞间通讯中发挥作用。在包括感染、恶性肿瘤和自身免疫性疾病（如类风湿关节炎（RA））在内的各种病理条件下，已报道 MPs 水平升高。RA 是一种自身免疫性系统性炎症性疾病，其特征为慢性滑膜炎症，导致软骨和骨损伤，加速动脉粥样硬化增加死亡率。根据文献数据，MPs 也可能在血管内皮功能障碍中发挥作用，导致 RA 患者的动脉粥样硬化。此外，许多研究人员已经表明，失调的自噬似乎参与了血管内皮功能障碍。自噬是一种修复过程，其中细胞质成分被隔离在双层膜囊泡中，并在与溶酶体隔室融合时降解。许多研究已经表明，基础自噬对于适当的血管功能是必不可少的。考虑到这些因素，我们假设在 RA 患者中，MPs 可能通过失调的内皮自噬过程促进动脉粥样硬化过程。
