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坏死性凋亡的调节作用:一种控制鱼类疾病的潜在预防方法。

Modulatory effects of necroptosis: A potential preventive approach to control diseases in fish.

机构信息

College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang, 453003, Henan, PR China.

College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang, 453003, Henan, PR China.

出版信息

Fish Shellfish Immunol. 2024 Sep;152:109802. doi: 10.1016/j.fsi.2024.109802. Epub 2024 Aug 3.

DOI:10.1016/j.fsi.2024.109802
PMID:39096982
Abstract

Necroptosis is a caspase-independent programmed cell death process characterized by morphological similarities to necrosis and the potential to cause significant inflammatory reactions. The initiation, execution, and inhibition of necroptosis involve a complex interplay of various signaling proteins. When death receptors bind to ligands, necroptosis is triggered through the receptor-interacting serine/threonine-protein kinase 1 (RIPK1)/RIPK3/Mixed Lineage Kinase Domain-Like (MLKL) axis, leading to inflammatory reactions in the surrounding tissues. This process encompasses numerous physiological regulatory mechanisms and contributes to the development and progression of certain diseases. The mechanisms of necroptosis were not well conserved across terrestrial and aquatic organisms, with differences in some components and functions. Given the significant challenges that aquatic animal diseases pose to aquaculture, research interest in necroptosis has surged recently, particularly in studies focusing on fish. Understanding necroptosis in fish can lead to interventions that offer potential breakthroughs in disease inhibition and fish health improvement.

摘要

细胞程序性坏死是一种不依赖于半胱天冬酶的细胞死亡过程,其形态学特征与坏死相似,并可能引发严重的炎症反应。细胞程序性坏死的起始、执行和抑制涉及各种信号蛋白的复杂相互作用。当死亡受体与配体结合时,细胞程序性坏死通过受体相互作用丝氨酸/苏氨酸蛋白激酶 1(RIPK1)/RIPK3/混合谱系激酶结构域样(MLKL)轴触发,导致周围组织发生炎症反应。这一过程包含许多生理调节机制,并有助于某些疾病的发生和发展。细胞程序性坏死的机制在陆地和水生生物中并不完全保守,某些成分和功能存在差异。鉴于水生动物疾病对水产养殖构成的重大挑战,最近对细胞程序性坏死的研究兴趣大增,尤其是在鱼类研究方面。了解鱼类的细胞程序性坏死可以为疾病抑制和鱼类健康改善提供潜在的突破。

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