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炎性小体受结直肠癌信号转导中表观遗传和自噬机制的影响。

Inflammasomes Are Influenced by Epigenetic and Autophagy Mechanisms in Colorectal Cancer Signaling.

机构信息

Immunology Division, Department of Internal Medicine and Hematology, Semmelweis University, 1088 Budapest, Hungary.

出版信息

Int J Mol Sci. 2024 Jun 3;25(11):6167. doi: 10.3390/ijms25116167.

Abstract

Inflammasomes contribute to colorectal cancer signaling by primarily inducing inflammation in the surrounding tumor microenvironment. Its role in inflammation is receiving increasing attention, as inflammation has a protumor effect in addition to inducing tissue damage. The inflammasome's function is complex and controlled by several layers of regulation. Epigenetic processes impact the functioning or manifestation of genes that are involved in the control of inflammasomes or the subsequent signaling cascades. Researchers have intensively studied the significance of epigenetic mechanisms in regulation, as they encompass several potential therapeutic targets. The regulatory interactions between the inflammasome and autophagy are intricate, exhibiting both advantageous and harmful consequences. The regulatory aspects between the two entities also encompass several therapeutic targets. The relationship between the activation of the inflammasome, autophagy, and epigenetic alterations in CRC is complex and involves several interrelated pathways. This article provides a brief summary of the newest studies on how epigenetics and autophagy control the inflammasome, with a special focus on their role in colorectal cancer. Based on the latest findings, we also provide an overview of the latest therapeutic ideas for this complex network.

摘要

炎症小体主要通过诱导周围肿瘤微环境中的炎症来促进结直肠癌信号转导。除了引起组织损伤外,炎症还具有促肿瘤作用,因此其在炎症中的作用越来越受到关注。炎症小体的功能复杂,受多层调控的控制。表观遗传过程影响参与炎症小体或后续信号级联控制的基因的功能或表现。研究人员已经深入研究了表观遗传机制在调控中的意义,因为它们包含几个潜在的治疗靶点。炎症小体和自噬之间的调控相互作用复杂,既具有有益的后果,也具有有害的后果。两者之间的调控方面还包含几个治疗靶点。炎症小体的激活、自噬以及 CRC 中的表观遗传改变之间的关系复杂,涉及几个相互关联的途径。本文简要总结了最新的关于表观遗传学和自噬如何控制炎症小体的研究,特别关注它们在结直肠癌中的作用。基于最新的发现,我们还概述了这个复杂网络的最新治疗思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73a4/11173330/408e7a9acca1/ijms-25-06167-g001.jpg

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