Macrophage Function in the Pathogenesis of Non-alcoholic Fatty Liver Disease: The Mac Attack

Oates, Jarren R; McKell, Melanie C; Moreno‐Fernandez, Maria E.; Damen, Michelle S M A; Deepe, George S.; Qualls, Joseph E.; Divanovic, Senad

doi:10.3389/fimmu.2019.02893

Cited by 64 publications

(54 citation statements)

References 202 publications

(234 reference statements)

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“…At present, there is a high prevalence of NAFLD in the world, which has attracted increasing attention. NAFLD includes a series of diseases, from simple fatty liver to non-alcoholic steatohepatitis (NASH), which may develop into liver cirrhosis or even liver cancer (27). Studies have shown that in the past 10 years, NAFLD has been associated with liver related incidence rate or mortality (28,29).…”

Section: Discussionmentioning

confidence: 99%

CML/RAGE Signal Bridges a Common Pathogenesis Between Atherosclerosis and Non-alcoholic Fatty Liver

et al. 2020

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Non-alcoholic fatty liver disease (NAFLD) has become a common chronic disease in the world. NAFLD is not only a simple intrahepatic lesion, but also affects the occurrence of a variety of extrahepatic complications. In particular, cardiovascular complications are particularly serious, which is the main cause of death in patients with NAFLD. To study the relationship between NAFLD and AS may be a new way to improve the quality of life in patients with NAFLD. As we all known, inflammatory response plays an important role in the occurrence and development of NAFLD and AS. In this study, we found that the accumulation of Nε-carboxymethyllysine (CML) in the liver leads to hepatic steatosis. CML can induce the expression of interleukin (IL-1β), interleukin (IL-6), tumor necrosis factor (TNF-α), C-reactionprotein (CRP) by binding with advanced glycosylation end-product receptor (RAGE) and accelerate the development of AS. After silencing RAGE expression, the expression of pro-inflammatory cytokines was inhibited and liver and aorta pathological changes were relieved. In conclusion, CML/RAGE signal promotes the progression of non-alcoholic fatty liver disease and atherosclerosis. We hope to provide new ideas for the study of liver vascular dialogue in multi organ communication.

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Section: Discussionmentioning

confidence: 99%

CML/RAGE Signal Bridges a Common Pathogenesis Between Atherosclerosis and Non-alcoholic Fatty Liver

et al. 2020

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“…In response to those signals sent by hepatocytes, KCs also signaled back to the hepatocytes and regulated their fate ( 43 – 46 ) ( Figure 2 ). Firstly, activated KCs exerted actions via producing cytokines (e.g., IL-6, TNFα, and IL-1β) ( 47 ). TNFα allowed for the activation of caspase-8 in hepatocytes by binding to TNF receptor 1 (TNFR1), which not only triggered apoptotic caspase cascade directly but also induced mitochondrial dysfunction to amplify the signals indirectly ( 8 , 48 ).…”

Section: Interaction Between Liver Macrophages and Hepatocytesmentioning

confidence: 99%

Crosstalk Between Liver Macrophages and Surrounding Cells in Nonalcoholic Steatohepatitis

Zhou

Wang

et al. 2020

Front. Immunol.

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Nonalcoholic steatohepatitis (NASH), the advanced stage of nonalcoholic fatty liver disease (NAFLD), is emerging as a leading cause of progressive liver fibrosis and end-stage liver disease. Liver macrophages, mainly composed of Kupffer cells (KCs) and monocyte-derived macrophages (MoMFs), play a vital role in NASH progression and regression. Recent advances suggest that cell-cell communication is a fundamental feature of hepatic microenvironment. The reprogramming of cell-cell signaling between macrophages and surrounding cells contributes to the pathogenesis of NASH. In this review, we summarize the current knowledge of NASH regarding the composition of liver macrophages and their communication with surrounding cells, which are composed of hepatocytes, hepatic stellate cells (HSCs), liver sinusoidal endothelial cells (LSECs) and other immune cells. We also discuss the potential therapeutic strategies based on the level of macrophages.

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“…Accumulative experimental and clinical data demonstrate that macrophages have an important role in the initiation and progression of NAFLD. [3] , [4] , [5] , [6] , [7] , [8] , [9] KCs and infiltrating monocyte-derived macrophages (MDMs) are two hepatic macrophage populations that undergo expansion and functional changes during NASH development. 4 , 8 , [10] , [11] , [12] However, the driving factors that induce such changes in liver macrophages remain to be determined.…”

Section: Introductionmentioning

confidence: 99%

Macrophage-derived thrombospondin 1 promotes obesity-associated non-alcoholic fatty liver disease

Gwag

Mooli

et al. 2021

JHEP Reports

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Macrophage Function in the Pathogenesis of Non-alcoholic Fatty Liver Disease: The Mac Attack

Cited by 64 publications

References 202 publications

CML/RAGE Signal Bridges a Common Pathogenesis Between Atherosclerosis and Non-alcoholic Fatty Liver

CML/RAGE Signal Bridges a Common Pathogenesis Between Atherosclerosis and Non-alcoholic Fatty Liver

Crosstalk Between Liver Macrophages and Surrounding Cells in Nonalcoholic Steatohepatitis

Macrophage-derived thrombospondin 1 promotes obesity-associated non-alcoholic fatty liver disease

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