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      Lipid Metabolism in Macrophages: Focus on Atherosclerosis

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          Abstract

          Mechanisms of lipid homeostasis and its impairment are of crucial importance for atherogenesis, and their understanding is necessary for successful development of new therapeutic approaches. In the arterial wall, macrophages play a prominent role in intracellular lipid accumulation, giving rise to foam cells that populate growing atherosclerotic plaques. Under normal conditions, macrophages are able to process substantial amounts of lipids and cholesterol without critical overload of the catabolic processes. However, in atherosclerosis, these pathways become inefficient, leading to imbalance in cholesterol and lipid metabolism and disruption of cellular functions. In this review, we summarize the existing knowledge on the involvement of macrophage lipid metabolism in atherosclerosis development, including both the results of recent studies and classical concepts, and provide a detailed description of these processes from the moment of lipid uptake with lipoproteins to cholesterol efflux.

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          Triacylglycerol synthesis enzymes mediate lipid droplet growth by relocalizing from the ER to lipid droplets.

          Florian Wilfling, Huajin Wang, Joel T. Haas … (2013)
          Lipid droplets (LDs) store metabolic energy and membrane lipid precursors. With excess metabolic energy, cells synthesize triacylglycerol (TG) and form LDs that grow dramatically. It is unclear how TG synthesis relates to LD formation and growth. Here, we identify two LD subpopulations: smaller LDs of relatively constant size, and LDs that grow larger. The latter population contains isoenzymes for each step of TG synthesis. Glycerol-3-phosphate acyltransferase 4 (GPAT4), which catalyzes the first and rate-limiting step, relocalizes from the endoplasmic reticulum (ER) to a subset of forming LDs, where it becomes stably associated. ER-to-LD targeting of GPAT4 and other LD-localized TG synthesis isozymes is required for LD growth. Key features of GPAT4 ER-to-LD targeting and function in LD growth are conserved between Drosophila and mammalian cells. Our results explain how TG synthesis is coupled with LD growth and identify two distinct LD subpopulations based on their capacity for localized TG synthesis. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Foam cells in atherosclerosis.

            Xiao-Hua Yu, Yu-Chang Fu, Da-Wei Zhang … (2013)
            Atherosclerosis is a chronic disease characterized by the deposition of excessive cholesterol in the arterial intima. Macrophage foam cells play a critical role in the occurrence and development of atherosclerosis. The generation of these cells is associated with imbalance of cholesterol influx, esterification and efflux. CD36 and scavenger receptor class A (SR-A) are mainly responsible for uptake of lipoprotein-derived cholesterol by macrophages. Acyl coenzyme A:cholesterol acyltransferase-1 (ACAT1) and neutral cholesteryl ester hydrolase (nCEH) regulate cholesterol esterification. ATP-binding cassette transporters A1(ABCA1), ABCG1 and scavenger receptor BI (SR-BI) play crucial roles in macrophage cholesterol export. When inflow and esterification of cholesterol increase and/or its outflow decrease, the macrophages are ultimately transformed into lipid-laden foam cells, the prototypical cells in the atherosclerotic plaque. The aim of this review is to describe what is known about the mechanisms of cholesterol uptake, esterification and release in macrophages. An increased understanding of the process of macrophage foam cell formation will help to develop novel therapeutic interventions for atherosclerosis. Copyright © 2013 The Authors. Published by Elsevier B.V. All rights reserved.
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              The lipodystrophy protein seipin is found at endoplasmic reticulum lipid droplet junctions and is important for droplet morphology.

              Kimberly Szymanski, Derk D. Binns, René Bartz … (2007)
              Lipodystrophy is a disorder characterized by a loss of adipose tissue often accompanied by severe hypertriglyceridemia, insulin resistance, diabetes, and fatty liver. It can be inherited or acquired. The most severe inherited form is Berardinelli-Seip Congenital Lipodystrophy Type 2, associated with mutations in the BSCL2 gene. BSCL2 encodes seipin, the function of which has been entirely unknown. We now report the identification of yeast BSCL2/seipin through a screen to detect genes important for lipid droplet morphology. The absence of yeast seipin results in irregular lipid droplets often clustered alongside proliferated endoplasmic reticulum (ER); giant lipid droplets are also seen. Many small irregular lipid droplets are also apparent in fibroblasts from a BSCL2 patient. Human seipin can functionally replace yeast seipin, but a missense mutation in human seipin that causes lipodystrophy, or corresponding mutations in the yeast gene, render them unable to complement. Yeast seipin is localized in the ER, where it forms puncta. Almost all lipid droplets appear to be on the ER, and seipin is found at these junctions. Therefore, we hypothesize that seipin is important for droplet maintenance and perhaps assembly. In addition to detecting seipin, the screen identified 58 other genes whose deletions cause aberrant lipid droplets, including 2 genes encoding proteins known to activate lipin, a lipodystrophy locus in mice, and 16 other genes that are involved in endosomal-lysosomal trafficking. The genes identified in our screen should be of value in understanding the pathway of lipid droplet biogenesis and maintenance and the cause of some lipodystrophies.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomedicines
                Journal ID (iso-abbrev): Biomedicines
                Journal ID (publisher-id): biomedicines
                Title: Biomedicines
                Publisher: MDPI
                ISSN (Electronic): 2227-9059
                Publication date (Electronic): 01 August 2020
                Publication date Collection: August 2020
                Volume: 8
                Issue: 8
                Electronic Location Identifier: 262
                Affiliations
                [1 ]Research Institute of Human Morphology, Laboratory of Cellular and Molecular Pathology of Cardiovascular System, 3 Tsyurupy Str., 117418 Moscow, Russia; nafany905@ 123456gmail.com (V.A.K.); igor.sobenin@ 123456gmail.com (I.A.S.); a.h.opexob@ 123456gmail.com (A.N.O.)
                [2 ]Russian Medical Research Center of Cardiology, Institute of Experimental Cardiology, Laboratory of Medical Genetics, 15-a 3-rd Cherepkovskaya Str., 121552 Moscow, Russia
                [3 ]Sechenov First Moscow State Medical University, 119146 Moscow, Russia; egozavr-ch@ 123456mail.ru
                [4 ]Institute for Atherosclerosis Research, Skolkovo Innovative Center, 121609 Moscow, Russia; kate.ivanov@ 123456gmail.com
                [5 ]Institute of General Pathology and Pathophysiology, Laboratory of Angiopathology, 8 Baltiyskaya Str., 125315 Moscow, Russia
                Author notes
                [* ]Correspondence: vasily.sukhorukov@ 123456morfolhum.ru ; Tel.: +7-915-393-3263
                Author information
                https://orcid.org/0000-0002-0312-3773
                https://orcid.org/0000-0003-2096-3237
                https://orcid.org/0000-0003-3159-2881
                https://orcid.org/0000-0003-0978-6444
                https://orcid.org/0000-0002-3318-4681
                Article
                Publisher ID: biomedicines-08-00262
                DOI: 10.3390/biomedicines8080262
                PMC ID: 7459513
                PubMed ID: 32752275
                SO-VID: f51ee441-66ec-4db7-ad48-cd0d0012a549
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 22 June 2020
                Date accepted : 27 July 2020
                Categories
                Subject: Review

                Keywords: lipid metabolism,foam cell,macrophage,atherosclerosis,lipid droplet
                Data availability:
                Keywords: lipid metabolism, foam cell, macrophage, atherosclerosis, lipid droplet

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