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自身免疫性风湿性疾病和动脉粥样硬化中的巨噬细胞功能障碍。

Macrophage Dysfunction in Autoimmune Rheumatic Diseases and Atherosclerosis.

机构信息

Department of Systemic Rheumatic Diseases, V.A. Nasonova Research Institute of Rheumatology, Kashirskoe Shosse, 115522 Moscow, Russia.

Chair of Organization and Economy of Pharmacy, Institute of Pharmacy, A.P. Nelyubina, I.M. Sechenov First Moscow State Medical University (Sechenov University), 96k1 Ave. Vernadsky, 119526 Moscow, Russia.

出版信息

Int J Mol Sci. 2022 Apr 19;23(9):4513. doi: 10.3390/ijms23094513.

DOI:10.3390/ijms23094513
PMID:35562903
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9102949/
Abstract

One of the problems of modern medical science is cardiovascular pathology caused by atherosclerotic vascular lesions in patients with autoimmune rheumatic diseases (ARDs). The similarity between the mechanisms of the immunopathogenesis of ARD and chronic low-grade inflammation in atherosclerosis draws attention. According to modern concepts, chronic inflammation associated with uncontrolled activation of both innate and acquired immunity plays a fundamental role in all stages of ARDs and atherosclerotic processes. Macrophage monocytes play an important role among the numerous immune cells and mediators involved in the immunopathogenesis of both ARDs and atherosclerosis. An imbalance between M1-like and M2-like macrophages is considered one of the causes of ARDs. The study of a key pathogenetic factor in the development of autoimmune and atherosclerotic inflammation-activated monocyte/macrophages will deepen the knowledge of chronic inflammation pathogenesis.

摘要

现代医学的一个问题是自身免疫性风湿病 (ARD) 患者的动脉粥样硬化血管病变引起的心血管病理学。ARD 的免疫发病机制与动脉粥样硬化的慢性低度炎症之间的相似性引起了关注。根据现代概念,与先天和获得性免疫的不受控制的激活相关的慢性炎症在 ARD 和动脉粥样硬化过程的所有阶段都起着根本作用。在参与 ARD 和动脉粥样硬化发病机制的众多免疫细胞和介质中,单核细胞/巨噬细胞起着重要作用。M1 样和 M2 样巨噬细胞之间的失衡被认为是 ARD 的原因之一。研究自身免疫和动脉粥样硬化炎症激活的单核细胞/巨噬细胞的关键致病因素将加深对慢性炎症发病机制的认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd9/9102949/26aae0ce76a1/ijms-23-04513-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd9/9102949/9e575abd6308/ijms-23-04513-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd9/9102949/26aae0ce76a1/ijms-23-04513-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd9/9102949/9e575abd6308/ijms-23-04513-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd9/9102949/26aae0ce76a1/ijms-23-04513-g002.jpg

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