Macrophages and scavenger receptors in obesity‐associated non‐alcoholic liver fatty disease (NAFLD)

Petersen, Sine Kragh; Bilkei‐Gorzo, Orsolya; Govaere, Olivier; Härtlová, Anetta

doi:10.1111/sji.12971

Cited by 11 publications

(10 citation statements)

References 55 publications

(101 reference statements)

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“…We also analyzed macrophages in the liver as previous study has demonstrated that inflammation and monocyte recruitment is involved in steatohepatitis [21,22] and macrophages might be the mediators and drivers of chronic low-grade inflammation in NAFLD. [23] Staining of F4/80, a widely used macrophage marker, revealed that the macrophage infiltration in the liver was elevated by HFHSD, while such elevation was reversed by the FMD administration (Figure 4F). In addition, we analyzed the mRNA levels of a few representative inflammation markers in the liver tissue.…”

Section: Intermittent Application Of the Fmd Reduces Hepatic Steatosis And Macrophage Infiltration In Nafld Mouse Modelmentioning

confidence: 99%

Improvement of Non‐Alcoholic Fatty Liver Disease in Mice by Intermittent Use of a Fasting‐Mimicking Diet

Zhao

Bai

Wei

et al. 2021

Molecular Nutrition Food Res

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Scope: Liver plays a central role in maintaining lipid homeostasis which is dysregulated in non-alcoholic fatty liver disease (NAFLD) caused by overload of dietary fat, increase in lipid synthesis, and alteration of fatty acid oxidation in the liver. In this study, we aimed to investigate whether intermittent calorie restriction using a fasting-mimicking diet (FMD) is able to slow down the progression of NAFLD in mice. Methods and Results: This study analyzed the intervention activity of a FMD low in carbohydrate/protein but high in dietary fibers with a NAFLD mouse model induced by high-fat high-sucrose diet (HFHSD). Intermittent application of the FMD reduces HFHSD-induced obesity and glucose intolerance. The FMD decreases the size of adipocytes and elevates expression of lipolysis genes and HSL protein in white adipose tissue. HFHSD-induced lipid accumulation in the liver is reduced by the FMD, accompanied by a reduction of macrophage marker in the liver. RNA sequencing reveals that the expression of a number of genes involved in fatty acid oxidation is elevated by the FMD. Conclusion: The findings indicate that intermittent application of the FMD can improve NAFLD, at least in part, through increased lipolysis in white adipose tissue and elevated fatty acid oxidation in the liver.

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Section: Intermittent Application Of the Fmd Reduces Hepatic Steatosis And Macrophage Infiltration In Nafld Mouse Modelmentioning

confidence: 99%

Improvement of Non‐Alcoholic Fatty Liver Disease in Mice by Intermittent Use of a Fasting‐Mimicking Diet

Zhao

Bai

Wei

et al. 2021

Molecular Nutrition Food Res

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“…Scavenger receptors comprise another prototypical class of different surface receptors that recognize and internalize OSEs ( 67 ). Similar to TLRs, scavenger receptors bind oxidized and non-native LDL particles and contribute to the activation of macrophages in the context of inflammation ( 67 , 75 ). There are many different types of scavenger receptors, including CD36, scavenger receptor type A1 (SR-A1), SR-A2, SR-B1, CD68, and lectin-like oxidized LDL receptor 1 (LOX1) ( 67 ).…”

Section: Immune Recognition Of Oxidation-specific Epitopesmentioning

confidence: 99%

Oxidized Lipids: Common Immunogenic Drivers of Non-Alcoholic Fatty Liver Disease and Atherosclerosis

Hoebinger¹,

Rajcic²,

Hendrikx

2022

Front. Cardiovasc. Med.

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The prevalence of non-alcoholic fatty liver disease (NAFLD), ranging from simple steatosis to inflammatory steatohepatitis (NASH) and cirrhosis, continues to rise, making it one of the major chronic liver diseases and indications for liver transplantation worldwide. The pathological processes underlying NAFLD not only affect the liver but are also likely to have systemic effects. In fact, growing evidence indicates that patients with NAFLD are at increased risk for developing atherosclerosis. Indeed, cardiovascular complications are the leading cause of mortality in NAFLD patients. Here, we aim to address common pathophysiological molecular pathways involved in chronic fatty liver disease and atherosclerosis. In particular, we focus on the role of oxidized lipids and the formation of oxidation-specific epitopes, which are important targets of host immunity. Acting as metabolic danger signals, they drive pro-inflammatory processes and thus contribute to disease progression. Finally, we summarize encouraging studies indicating that oxidized lipids are promising immunological targets to improve intervention strategies for NAFLD and potentially limit the risk of developing atherosclerosis.

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“…Resistin can increase the uptake of oxidised lowdensity lipoprotein by macrophages through their scavenger receptors, thereby promoting foamy cell formation in vitro, suggesting that HPCs influence macrophage function [70][71][72] . Recently, our group showed that the formation of foamy macrophages in human NAFLD is mediated by the macrophage scavenger receptor 1, resulting in the release of pro-inflammatory cytokines, such as TNFa, but also inducing metabolic changes in the liver [73,74] . Adiponectin, on the other hand, is regarded as an anti-inflammatory modulator in NAFLD and is protective against HCC formation [69,75] .…”

Section: Hepatic Progenitor Cell Secretomementioning

confidence: 99%

Clinical implications of hepatic progenitor cell activation in non-alcoholic fatty liver disease

Younes¹,

Burgoyne²,

Tiniakos³

et al. 2021

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Non-alcoholic fatty liver disease (NAFLD) is one of the most prominent causes of liver-related morbidity in the Western world. NAFLD is a chronic disease characterised by accumulation of triglycerides in hepatocytes. Upon damage, hepatocytes drive regeneration to sustain homeostasis of the liver. However, 30-40 years of ongoing replication induced by chronic lipid damage and oxidative stress increase senescence of the hepatocytes. At this stage, activation of a reserve compartment is seen, known as the hepatic progenitor cells (HPCs). HPCs are bipotent cells which can differentiate into hepatocytes or cholangiocytes depending on the underlying aetiology in order to facilitate liver regeneration. Activation of HPCs is observed as ductular reaction (DR), comprising an expansion of transit amplifying cells of the terminal branches of the biliary tree. DR is usually observed in advanced NAFLD but is also associated with histological severity and distinct molecular profiles. In this context, information about HPCs and their activation in the form of DR may add a both diagnostic and prognostic values when assessing NAFLD patients. In this review, we analyse HPCs characteristics and development, and the clinical impact of their activation in subjects with NAFLD.

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Macrophages and scavenger receptors in obesity‐associated non‐alcoholic liver fatty disease (NAFLD)

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 11 publications

References 55 publications

Improvement of Non‐Alcoholic Fatty Liver Disease in Mice by Intermittent Use of a Fasting‐Mimicking Diet

Improvement of Non‐Alcoholic Fatty Liver Disease in Mice by Intermittent Use of a Fasting‐Mimicking Diet

Oxidized Lipids: Common Immunogenic Drivers of Non-Alcoholic Fatty Liver Disease and Atherosclerosis

Clinical implications of hepatic progenitor cell activation in non-alcoholic fatty liver disease

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