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细胞坏死性凋亡及其在炎症性肠病治疗靶点的作用

The Function of Necroptosis and Its Treatment Target in IBD.

机构信息

Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province Department of Laboratory Medicine School of Medicine Jiangsu University, Zhenjiang 212013, Jiangsu, China.

The People's Hospital of Danyang Affiliated Danyang Hospital of Nantong University, Zhenjiang 212300, Jiangsu, China.

出版信息

Mediators Inflamm. 2024 Jul 31;2024:7275309. doi: 10.1155/2024/7275309. eCollection 2024.

DOI:10.1155/2024/7275309
PMID:39118979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11306684/
Abstract

Inflammatory bowel disease (IBD), which encompasses Crohn's disease (CD) and ulcerative colitis (UC), is a complicated illness whose exact cause is yet unknown. Necroptosis is associated with IBD pathogenesis, leading to intestinal barrier abnormalities and uncontrolled inflammation. Molecules involved in necroptosis, however, exhibit different expression levels in IBD and its associated colorectal cancer. Multiple studies have shown that inhibiting these molecules alleviates necroptosis-induced IBD. Moreover, due to the severe scarcity of clinical medications for treating IBD caused by necroptosis, we review the various functions of crucial necroptosis molecules in IBD, the stimuli regulating necroptosis, and the current emerging therapeutic strategies for treating IBD-associated necroptosis. Eventually, understanding the pathogenesis of necroptosis in IBD will enable the development of additional therapeutic approaches for the illness.

摘要

炎症性肠病(IBD)包括克罗恩病(CD)和溃疡性结肠炎(UC),是一种复杂的疾病,其确切病因尚不清楚。细胞坏死性凋亡与 IBD 的发病机制有关,导致肠道屏障异常和失控性炎症。然而,参与细胞坏死性凋亡的分子在 IBD 及其相关结直肠癌中的表达水平不同。多项研究表明,抑制这些分子可减轻细胞坏死性凋亡诱导的 IBD。此外,由于治疗由细胞坏死性凋亡引起的 IBD 的临床药物严重缺乏,我们综述了关键细胞坏死性凋亡分子在 IBD 中的各种功能、调节细胞坏死性凋亡的刺激因素以及治疗与细胞坏死性凋亡相关的 IBD 的新兴治疗策略。最终,了解细胞坏死性凋亡在 IBD 中的发病机制将为该疾病的治疗方法的发展提供更多的机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54d3/11306684/2e5f0b990b60/MI2024-7275309.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54d3/11306684/0723e401affb/MI2024-7275309.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54d3/11306684/cc75f726b59c/MI2024-7275309.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54d3/11306684/2e5f0b990b60/MI2024-7275309.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54d3/11306684/0723e401affb/MI2024-7275309.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54d3/11306684/cc75f726b59c/MI2024-7275309.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54d3/11306684/2e5f0b990b60/MI2024-7275309.003.jpg

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Tissue Cell. 2024 Apr;87:102323. doi: 10.1016/j.tice.2024.102323. Epub 2024 Feb 4.
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ALOX5 drives the pyroptosis of CD4 T cells and tissue inflammation in rheumatoid arthritis.ALOX5 驱动类风湿关节炎中 CD4 T 细胞的细胞焦亡和组织炎症。
Sci Signal. 2024 Feb 27;17(825):eadh1178. doi: 10.1126/scisignal.adh1178.
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Macrophage Tim-3 maintains intestinal homeostasis in DSS-induced colitis by suppressing neutrophil necroptosis.
靶向MCF-7乳腺癌细胞中的坏死性凋亡:通过分子对接、动力学、密度泛函理论和分子静电势研究对血水草中8,12-二甲氧基血根碱的计算机模拟见解。
PLoS One. 2025 Jan 7;20(1):e0313094. doi: 10.1371/journal.pone.0313094. eCollection 2025.
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Redox Biol. 2024 Apr;70:103072. doi: 10.1016/j.redox.2024.103072. Epub 2024 Feb 2.
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Early-life diet and risk of inflammatory bowel disease: a pooled study in two Scandinavian birth cohorts.早期生活饮食与炎症性肠病风险:两个斯堪的纳维亚出生队列的汇总研究。
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