Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response

The endoplasmic reticulum (ER) stress is an important event in the pathogenesis of different human disorders, including atherosclerosis. ER stress leads to disturbance of cellular homeostasis, apoptosis, and in the case of macrophages, to foam cell formation and pro-inflammatory cytokines production...

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Main Authors: Vasily N. Sukhorukov, Victoria A. Khotina, Mariam Bagheri Ekta, Ekaterina A. Ivanova, Igor A. Sobenin, Alexander N. Orekhov
Format: Article
Language:English
Published: MDPI AG 2020-07-01
Series:Biomedicines
Subjects:
Online Access:https://www.mdpi.com/2227-9059/8/7/210
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author Vasily N. Sukhorukov
Victoria A. Khotina
Mariam Bagheri Ekta
Ekaterina A. Ivanova
Igor A. Sobenin
Alexander N. Orekhov
author_facet Vasily N. Sukhorukov
Victoria A. Khotina
Mariam Bagheri Ekta
Ekaterina A. Ivanova
Igor A. Sobenin
Alexander N. Orekhov
author_sort Vasily N. Sukhorukov
collection DOAJ
description The endoplasmic reticulum (ER) stress is an important event in the pathogenesis of different human disorders, including atherosclerosis. ER stress leads to disturbance of cellular homeostasis, apoptosis, and in the case of macrophages, to foam cell formation and pro-inflammatory cytokines production. In atherosclerosis, several cell types can be affected by ER stress, including endothelial cells, vascular smooth muscular cells, and macrophages. Modified low-density lipoproteins (LDL) and cytokines, in turn, can provoke ER stress through different processes. The signaling cascades involved in ER stress initiation are complex and linked to other cellular processes, such as lysosomal biogenesis and functioning, autophagy, mitochondrial homeostasis, and energy production. In this review, we discuss the underlying mechanisms of ER stress formation and the interplay of lipid accumulation and pro-inflammatory response. We will specifically focus on macrophages, which are the key players in maintaining chronic inflammatory milieu in atherosclerotic lesions, and also a major source of lipid-accumulating foam cells.
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spelling doaj.art-cf3e4fae8ac043a299236f76a80f7bf62023-11-20T06:40:00ZengMDPI AGBiomedicines2227-90592020-07-018721010.3390/biomedicines8070210Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory ResponseVasily N. Sukhorukov0Victoria A. Khotina1Mariam Bagheri Ekta2Ekaterina A. Ivanova3Igor A. Sobenin4Alexander N. Orekhov5Research Institute of Human Morphology, Laboratory of Cellular and Molecular Pathology of Cardiovascular System, 3 Tsyurupy Str., 117418 Moscow, RussiaResearch Institute of Human Morphology, Laboratory of Cellular and Molecular Pathology of Cardiovascular System, 3 Tsyurupy Str., 117418 Moscow, RussiaResearch Institute of Human Morphology, Laboratory of Cellular and Molecular Pathology of Cardiovascular System, 3 Tsyurupy Str., 117418 Moscow, RussiaInstitute for Atherosclerosis Research, Skolkovo Innovative Center, 121609 Moscow, RussiaResearch Institute of Human Morphology, Laboratory of Cellular and Molecular Pathology of Cardiovascular System, 3 Tsyurupy Str., 117418 Moscow, RussiaResearch Institute of Human Morphology, Laboratory of Cellular and Molecular Pathology of Cardiovascular System, 3 Tsyurupy Str., 117418 Moscow, RussiaThe endoplasmic reticulum (ER) stress is an important event in the pathogenesis of different human disorders, including atherosclerosis. ER stress leads to disturbance of cellular homeostasis, apoptosis, and in the case of macrophages, to foam cell formation and pro-inflammatory cytokines production. In atherosclerosis, several cell types can be affected by ER stress, including endothelial cells, vascular smooth muscular cells, and macrophages. Modified low-density lipoproteins (LDL) and cytokines, in turn, can provoke ER stress through different processes. The signaling cascades involved in ER stress initiation are complex and linked to other cellular processes, such as lysosomal biogenesis and functioning, autophagy, mitochondrial homeostasis, and energy production. In this review, we discuss the underlying mechanisms of ER stress formation and the interplay of lipid accumulation and pro-inflammatory response. We will specifically focus on macrophages, which are the key players in maintaining chronic inflammatory milieu in atherosclerotic lesions, and also a major source of lipid-accumulating foam cells.https://www.mdpi.com/2227-9059/8/7/210atherosclerosisendoplasmic reticulum stressmacrophagespro-inflammatory responsefoam cells
spellingShingle Vasily N. Sukhorukov
Victoria A. Khotina
Mariam Bagheri Ekta
Ekaterina A. Ivanova
Igor A. Sobenin
Alexander N. Orekhov
Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response
Biomedicines
atherosclerosis
endoplasmic reticulum stress
macrophages
pro-inflammatory response
foam cells
title Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response
title_full Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response
title_fullStr Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response
title_full_unstemmed Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response
title_short Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response
title_sort endoplasmic reticulum stress in macrophages the vicious circle of lipid accumulation and pro inflammatory response
topic atherosclerosis
endoplasmic reticulum stress
macrophages
pro-inflammatory response
foam cells
url https://www.mdpi.com/2227-9059/8/7/210
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