Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
J Immunol Res. 2017;2017:8160589. doi: 10.1155/2017/8160589. Epub 2017 Dec 27.
Cerebral aneurysms (CAs) have become a health burden not only because their rupture is life threatening, but for a series of devastating complications left in survivors. It is well accepted that sustained chronic inflammation plays a crucial role in the pathology of cerebral aneurysms. In particular, macrophages have been identified as critical effector cells orchestrating inflammation in CAs. In recent years, dysregulated M1/M2 polarization has been proposed to participate in the progression of CAs. Although the pathological mechanisms of M1/M2 imbalance in CAs remain largely unknown, recent advances have been made in the understanding of the molecular basis and other immune cells involving in this sophisticated network. We provide a concise overview of the mechanisms associated with macrophage plasticity and the emerging molecular targets.
脑动脉瘤（CAs）不仅因其破裂具有生命威胁性，而且还因其给幸存者带来一系列毁灭性的并发症，成为了健康负担。目前公认的是，持续的慢性炎症在脑动脉瘤的病理过程中起着关键作用。特别是，巨噬细胞已被确定为在 CAs 中协调炎症的关键效应细胞。近年来，失调的 M1/M2 极化被认为参与了 CAs 的进展。尽管 CAs 中 M1/M2 失衡的病理机制在很大程度上仍不清楚，但在理解涉及这一复杂网络的分子基础和其他免疫细胞方面已经取得了一些进展。我们简要概述了与巨噬细胞可塑性和新兴分子靶点相关的机制。
