神经退行性疾病中的炎症酶
Qianchen Wang1, Songwei Yang2, Xuan Zhang3
1Department of Pharmacy, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Translational neurodegeneration
|December 22, 2024
概括
炎症细胞,关键的先天免疫传感器,激活在神经退行性疾病由于错误折叠的蛋白质. 这导致炎症和细胞死亡,突出显示了炎症体作为潜在的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 神经科学是一个神经科学.
- 分子生物学分子生物学
背景情况:
- 炎症细胞是天生的免疫传感器,可以识别病原体相关的分子模式 (PAMPs) 和损伤相关的分子模式 (DAMPs).
- 神经退行性疾病中的β-粉样蛋白和α-synuclein等错误折叠的蛋白质触发了炎症酶激活.
- 激活的炎症体释放出促炎性细胞因子 (IL-1β,IL-18) 并诱导热,加剧神经炎症.
研究的目的:
- 审查炎症酶在神经退行性疾病中的作用.
- 在这些条件下,专注于正规的炎症酶激活途径.
- 讨论炎症体作为神经退行性疾病的潜在治疗点.
主要方法:
- 文献综述专注于神经退行性疾病中的炎症酶激活.
- 对正规炎症酶途径参与的证据分析.
- 综合当前对炎症体作用和治疗潜力的理解.
主要成果:
- 炎症酶激活越来越多地与神经退行性疾病的发病有关.
- 规范性炎症体通路经常参与与疾病相关的炎症体激活.
- 炎症酶诱导的热和细胞因子释放对神经炎症有显著的贡献.
结论:
- 炎症酶在与神经退行性疾病相关的神经炎症中发挥着关键作用.
- 了解炎症酶激活机制对于开发有效治疗方法至关重要.
- 针对炎症细胞提供了一个有前途的治疗策略,用于神经退行性疾病.
相关概念视频
Caspases
12.3K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
12.3K
Amyloid Fibrils
9.2K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
9.2K
Inflammation
52.5K
Overview
52.5K
NF-κB-dependent Signaling Pathway
7.2K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
7.2K
Phagocytosis of Apoptotic Cells
3.7K
Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized...
Normal cells contain receptors that prevent them from being recognized...
3.7K
The Intrinsic Apoptotic Pathway
6.4K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.4K


