首页|AIM在炎症反应和脂质代谢疾病中的作用

AIM在炎症反应和脂质代谢疾病中的作用

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巨噬细胞凋亡抑制因子(apoptosis inhibitor of macrophage,AIM),是清道夫受体富含半胱氨酸残基超家族(scavenger receptor cysteine rich-super family,SRCR-SF)B 组的成员之一。AIM 为巨噬细胞分泌的一种可溶性蛋白,该蛋白的表达受肝X受体(liver X receptor,LXR)控制,且在机体的免疫反应中起重要作用。AIM作为巨噬细胞的一种分泌蛋白,发挥着广泛的作用,不仅对巨噬细胞的凋亡具有抑制作用,并且可参与调控巨噬细胞极化。还有相关研究发现,AIM参与炎症、肥胖、动脉粥样硬化和癌症等多种生理、病理过程;可以作为结核病和肝硬化等疾病的生物诊断标志物;可以通过抑制脂肪酸合成酶(fatty acid synthase,FAS)活性从而促进脂肪细胞的脂解,在调节脂质内稳态平衡、脂质代谢与自身免疫疾病中发挥着重要的作用。该文论述了 AIM的分子特征及其在炎症反应和脂质代谢等相关疾病方面的作用,展示AIM的多种功能特点,为相关的医学研究提供依据。
Effect of apoptosis inhibitor of macrophage in inflammatory reactions and lipid metabolic diseases
Apoptosis inhibitor of macrophage(AIM)belongs to group B of the scavenger receptor cysteine rich-super family.AIM is a soluble protein secreted by macrophages.The expression of this protein is controlled by the liver X receptor.AIM,which is secreted by macrophages,plays important and broad roles in the immune responses of the body.It not only inhibits the apoptosis of macrophages but also participates in the regulation of macrophage polarization.In addition,studies have revealed that AIM is involved in various physiological and pathological processes,such as inflammation,obesity,atherosclerosis,and cancer.It has been used as a biological marker for the diagnosis of diseases such as tuberculosis and liver cirrhosis.Moreover,it can promote the lipolysis of adipose cells by inhibiting the activity of fatty acid synthase(FAS),playing an important role in the regulation of lipid homeostasis,lipid metabolism,and autoimmune diseases.In this paper,we review the multiple functional characteristics of AIM and its effects on inflammation,lipid metabolism,and related diseases to provide a theoretical basis for relevant medical research.

AIMinflammatory reactionlipid metabolism

张帆、田春雨、王景存、喇孝瑾、付茜茹、李洁、付文浩

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华北理工大学,河北唐山 063210

河北省中西医结合防治糖尿病及其并发症重点实验室,河北唐山 063210

AIM 炎症反应 脂质代谢

河北省自然科学基金河北省中医药局科技项目唐山市科技计划

H2020209235202313722130219H

2024

中国比较医学杂志
中国实验动物学会,中国医学科学院医学实验动物研究所

中国比较医学杂志

CSTPCD北大核心
影响因子:0.473
ISSN:1671-7856
年,卷(期):2024.34(3)
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