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胞葬作用:动脉粥样硬化斑块逆转的一颗新星。

Efferocytosis: A new star of atherosclerotic plaques reversal.

作者信息

Liang Xiangyu, Tian Shuoqi, Zhang Han, Sun Shusen, Zhang Peixiang, Li Jiameng, Li Yong, Zhang Yanfen, Liu Zhongcheng

机构信息

College of Pharmaceutical Sciences, Key Laboratory of Pharmaceutical Quality Control of Hebei Province, Hebei University, Baoding, China; State Key Laboratory of New Pharmaceutical Preparations and Excipients, Baoding, China.

Beijing Yongkang Nian Health Technology Co., Ltd., Beijing, China.

出版信息

Int Immunopharmacol. 2025 Jan 27;146:113904. doi: 10.1016/j.intimp.2024.113904. Epub 2024 Dec 26.

Abstract

Efferocytosis is considered the key to eliminate apoptotic cells (ACs) under physiological and pathological conditions in vivo, mainly through different types of macrophages to achieve this process. Especially, tissue-resident macrophages (TRMs) are very significant for inflammation regression and maintenance of homeostasis in vivo. Abnormal efferocytosis will lead to the accumulation of ACs and the release of a variety of pro-inflammatory factors, which mediates the occurrence of many inflammatory diseases, including atherosclerosis (AS). AS is a chronic inflammatory vascular disease with the participation of the immune system. Defective efferocytosis will accelerate the progress of AS to a certain extent. Therefore, it is of great significance to understand the mechanism of efferocytosis and realize the prevention and treatment of AS through efferocytosis. In this review, we will briefly describe the specific process of efferocytosis, deeply discuss the possible molecular mechanism of impaired efferocytosis promoting the development of AS, and summarize the ways to prevent and treat AS through efferocytosis intervention therapy.

摘要

在体内生理和病理条件下,噬菌作用被认为是清除凋亡细胞(ACs)的关键,主要通过不同类型的巨噬细胞来完成这一过程。特别是,组织驻留巨噬细胞(TRMs)对于体内炎症消退和内环境稳态的维持非常重要。异常的噬菌作用会导致ACs的积累和多种促炎因子的释放,这介导了许多炎症性疾病的发生,包括动脉粥样硬化(AS)。AS是一种有免疫系统参与的慢性炎症性血管疾病。有缺陷的噬菌作用会在一定程度上加速AS的进展。因此,了解噬菌作用的机制并通过噬菌作用实现AS的防治具有重要意义。在这篇综述中,我们将简要描述噬菌作用的具体过程,深入探讨噬菌作用受损促进AS发展的可能分子机制,并总结通过噬菌作用干预疗法防治AS的方法。

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