Wang Qianchen, Yang Songwei, Zhang Xuan, Zhang Shanshan, Chen Liping, Wang Wanxue, Chen Naihong, Yan Jiaqing
Department of Pharmacy, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Hunan Engineering Technology Center of Standardization and Function of Chinese Herbal Decoction Pieces, School of Pharmacy, Hunan University of Chinese Medicine, Changsha, 410208, China.
Transl Neurodegener. 2024 Dec 23;13(1):65. doi: 10.1186/s40035-024-00459-0.
Inflammasomes represent a crucial component of the innate immune system, which respond to threats by recognizing different molecules. These are known as pathogen-associated molecular patterns (PAMPs) or host-derived damage-associated molecular patterns (DAMPs). In neurodegenerative diseases and neuroinflammation, the accumulation of misfolded proteins, such as beta-amyloid and alpha-synuclein, can lead to inflammasome activation, resulting in the release of interleukin (IL)-1β and IL-18. This activation also induces pyroptosis, the release of inflammatory mediators, and exacerbates neuroinflammation. Increasing evidence suggests that inflammasomes play a pivotal role in neurodegenerative diseases. Therefore, elucidating and investigating the activation and regulation of inflammasomes in these diseases is of paramount importance. This review is primarily focused on evidence indicating that inflammasomes are activated through the canonical pathway in these diseases. Inflammasomes as potential targets for treating neurodegenerative diseases are also discussed.
炎性小体是固有免疫系统的关键组成部分,其通过识别不同分子对威胁做出反应。这些分子被称为病原体相关分子模式(PAMPs)或宿主来源的损伤相关分子模式(DAMPs)。在神经退行性疾病和神经炎症中,错误折叠蛋白(如β-淀粉样蛋白和α-突触核蛋白)的积累可导致炎性小体激活,从而导致白细胞介素(IL)-1β和IL-18的释放。这种激活还会诱导细胞焦亡、炎性介质的释放,并加剧神经炎症。越来越多的证据表明,炎性小体在神经退行性疾病中起关键作用。因此,阐明和研究这些疾病中炎性小体的激活和调节至关重要。本综述主要关注表明炎性小体在这些疾病中通过经典途径被激活的证据。还讨论了炎性小体作为治疗神经退行性疾病潜在靶点的相关内容。