The Crosstalk between Autophagy and Polarization of Macrophages in Atherosclerosis
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- 英文论文题名：The Crosstalk between Autophagy and Polarization of Macrophages in Atherosclerosis
- 论文作者：Chen Wenna ; Wang Dan ; Wang Junyan ; Jia Lianqun
- 英文论文作者：Chen Wenna ; Wang Dan ; Wang Junyan ; Jia Lianqun ; Liaoning University of Traditional Chinese Medicine
- 年：2016
- 作者机构：Liaoning University of Traditional Chinese Medicine;
- 英文论文关键词：Macrophage ; Autophagy ; Polarization ; Signal pathway
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R543.5
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：270k
- 原文格式：D
- 会议级别：全国
摘要
In the past few years, researchers are attempting to understand in detail the role of macrophages in initiating and sustaining atherosclerosis, with the goal of learning how to reverse these events. Here, we respect to the polarization of macrophages associated with autophagy from the initiation of atherosclerotic plaques to its progression and regression, discussing the roles of macrophages play at these different disease stages. From the previous research, we find that the polarization and autophagy of M1 and M2 macrophages are distinct to induce opposite function and cellular metabolism in atherosclerotic plaques. Whereas both of them could be modulated by respective signal pathway, such as SmadGSK3β-PI3K-Akt-mTOR, GSK3β-Jak/STAT, GSK3β-WNT-SHH, or Jak/Stat-PI3K-Akt-mTOR, and mTOR is the key target on these cascades(Figure1). By the crosstalk of mTOR, it could enhance M2 macrophage autophagy to promote ox-LDL breakdown to liberate free fatty acids(FFA) and cholesterol through the pathway of RCT, which fuel oxidative metabolism and cholesterol efflux. While in M1 macrophages, it could induce defective autophagy which is associated with inflammasome hyperactivation, increased IL-1β production, and a buildup of cholesterol crystals. Macrophage autophagy is important for efficient efferocytosis of apoptotic plaque macrophages. Therefore, autophagy appears to be an important process in the reparative M2 macrophage phenotype in the process of formation of atherosclerotic plaques, whereas defective autophagy in macrophages may contribute to the less beneficial M1 phenotypic change.
In the past few years, researchers are attempting to understand in detail the role of macrophages in initiating and sustaining atherosclerosis, with the goal of learning how to reverse these events. Here, we respect to the polarization of macrophages associated with autophagy from the initiation of atherosclerotic plaques to its progression and regression, discussing the roles of macrophages play at these different disease stages. From the previous research, we find that the polarization and autophagy of M1 and M2 macrophages are distinct to induce opposite function and cellular metabolism in atherosclerotic plaques. Whereas both of them could be modulated by respective signal pathway, such as SmadGSK3β-PI3K-Akt-mTOR, GSK3β-Jak/STAT, GSK3β-WNT-SHH, or Jak/Stat-PI3K-Akt-mTOR, and mTOR is the key target on these cascades(Figure1). By the crosstalk of mTOR, it could enhance M2 macrophage autophagy to promote ox-LDL breakdown to liberate free fatty acids(FFA) and cholesterol through the pathway of RCT, which fuel oxidative metabolism and cholesterol efflux. While in M1 macrophages, it could induce defective autophagy which is associated with inflammasome hyperactivation, increased IL-1β production, and a buildup of cholesterol crystals. Macrophage autophagy is important for efficient efferocytosis of apoptotic plaque macrophages. Therefore, autophagy appears to be an important process in the reparative M2 macrophage phenotype in the process of formation of atherosclerotic plaques, whereas defective autophagy in macrophages may contribute to the less beneficial M1 phenotypic change.
In the past few years, researchers are attempting to understand in detail the role of macrophages in initiating and sustaining atherosclerosis, with the goal of learning how to reverse these events. Here, we respect to the polarization of macrophages associated with autophagy from the initiation of atherosclerotic plaques to its progression and regression, discussing the roles of macrophages play at these different disease stages. From the previous research, we find that the polarization and autophagy of M1 and M2 macrophages are distinct to induce opposite function and cellular metabolism in atherosclerotic plaques. Whereas both of them could be modulated by respective signal pathway, such as SmadGSK3β-PI3K-Akt-mTOR, GSK3β-Jak/STAT, GSK3β-WNT-SHH, or Jak/Stat-PI3K-Akt-mTOR, and mTOR is the key target on these cascades(Figure1). By the crosstalk of mTOR, it could enhance M2 macrophage autophagy to promote ox-LDL breakdown to liberate free fatty acids(FFA) and cholesterol through the pathway of RCT, which fuel oxidative metabolism and cholesterol efflux. While in M1 macrophages, it could induce defective autophagy which is associated with inflammasome hyperactivation, increased IL-1β production, and a buildup of cholesterol crystals. Macrophage autophagy is important for efficient efferocytosis of apoptotic plaque macrophages. Therefore, autophagy appears to be an important process in the reparative M2 macrophage phenotype in the process of formation of atherosclerotic plaques, whereas defective autophagy in macrophages may contribute to the less beneficial M1 phenotypic change.
引文