Department of Orthodontics, Medical University of Lodz, 92-216 Lodz, Poland.
Department of Pediatric Dentistry, Medical University of Lodz, 92-216 Lodz, Poland.
Int J Mol Sci. 2018 Apr 19;19(4):1245. doi: 10.3390/ijms19041245.
The rupture of saccular intracranial aneurysms (IA) is the commonest cause of non-traumatic subarachnoid hemorrhage (SAH)—the most serious form of stroke with a high mortality rate. Aneurysm walls are usually characterized by an active inflammatory response, and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) has been identified as the main transcription factor regulating the induction of inflammation-related genes in IA lesions. This transcription factor has also been related to IA rupture and resulting SAH. We and others have shown that autophagy interacts with inflammation in many diseases, but there is no information of such interplay in IA. Moreover, NF-κB, which is a pivotal factor controlling inflammation, is regulated by autophagy-related proteins, and autophagy is regulated by NF-κB signaling. It was also shown that autophagy mediates the normal functioning of vessels, so its disturbance can be associated with vessel-related disorders. Early brain injury, delayed brain injury, and associated cerebral vasospasm are among the most serious consequences of IA rupture and are associated with impaired function of the autophagy⁻lysosomal system. Further studies on the role of the interplay between autophagy and NF-κB-mediated inflammation in IA can help to better understand IA pathogenesis and to identify IA patients with an increased SAH risk.
囊状颅内动脉瘤（IA）破裂是创伤性蛛网膜下腔出血（SAH）——最严重的中风类型之一，死亡率很高的常见原因。动脉瘤壁通常以活跃的炎症反应为特征，NF-κB（核因子κB）已被确定为调节 IA 病变中炎症相关基因诱导的主要转录因子。该转录因子也与 IA 破裂和由此导致的 SAH 有关。我们和其他人已经表明，自噬在许多疾病中与炎症相互作用，但在 IA 中没有这种相互作用的信息。此外，NF-κB 是控制炎症的关键因素，它受自噬相关蛋白的调节，而自噬受 NF-κB 信号的调节。还表明自噬介导了血管的正常功能，因此其紊乱可能与血管相关疾病有关。早期脑损伤、迟发性脑损伤和相关的脑血管痉挛是 IA 破裂的最严重后果之一，与自噬溶酶体系统功能受损有关。进一步研究自噬与 NF-κB 介导的炎症之间相互作用的作用，有助于更好地了解 IA 的发病机制，并识别出 SAH 风险增加的 IA 患者。
