实用医学杂志 ›› 2024, Vol. 40 ›› Issue (23): 3419-3426.doi: 10.3969/j.issn.1006-5725.2024.23.022
• 综述 • 上一篇
肖潇1,龙方懿2,王刚1
收稿日期:
2024-09-02
出版日期:
2024-12-10
发布日期:
2024-12-16
通讯作者:
王刚
基金资助:
Xiao XIAO1,Fangyi LONG2,Gang. WANG1
Received:
2024-09-02
Online:
2024-12-10
Published:
2024-12-16
Contact:
Gang. WANG
摘要:
细胞焦亡(pyroptosis)是一种具有炎症特征的程序性细胞死亡方式,近年来在生物医学领域引起了广泛关注。细胞焦亡在激活宿主防御、促进炎症反应、调节免疫应答及影响肿瘤微环境等方面发挥重要作用。在癌症的研究中,细胞焦亡的双重作用尤为显著,它既可以抑制肿瘤生长,也能在某些情况下促进肿瘤的发展。此外,对细胞焦亡的研究为癌症治疗提供了新的视角,特别是在增强传统放化疗效果、促进抗肿瘤免疫反应以及开发纳米治疗策略方面,细胞焦亡的机制为新研究途径提供了基础。该文综述了细胞焦亡在癌症进展中的调控作用,以及其作为潜在抗癌策略的理论基础和实际应用进展,期望为未来癌症治疗策略的发展提供新的思路和方向。
中图分类号:
肖潇,龙方懿,王刚. 细胞焦亡在癌症治疗中的双重作用与新策略[J]. 实用医学杂志, 2024, 40(23): 3419-3426.
Xiao XIAO,Fangyi LONG,Gang. WANG. Dual role and new strategies of pyroptosis in cancer therapy[J]. The Journal of Practical Medicine, 2024, 40(23): 3419-3426.
图1
细胞焦亡的两种主要途径注:A,依赖Caspase-1的经典途径。在经典途径中,病原体或内源性危险信号分别触发NLRP1、NLRP3、NLRC4、AIM2等模式识别受体(PRR),并与接头蛋白ASC和无活性的Caspase-1前体(Pro-caspase-1)组装形成炎性小体复合物。随后,活化的Caspase-1裂解GSDMD和Pro-IL1β/Pro-IL18,GSDMD的N端结构域(GSDMD-NT)在质膜中形成非选择性孔隙,并释放细胞内容物,从而执行细胞焦亡。B,依赖Caspase-4/5/11的非经典途径。细胞外革兰阴性菌的脂多糖(LPS)直接激活Pro-caspase-4/5/11,这些活化的Caspase进一步裂解GSDMD生成GSDMD-NT,从而触发细胞焦亡(本图由Figdraw绘制)"
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