Nonalcoholic Fatty Liver Disease

Ding, Lingling; Oligschlaeger, Yvonne; Shiri-Sverdlov, Ronit; Houben, Tom

doi:10.1007/164_2020_352

Cited by 10 publications

(20 citation statements)

References 307 publications

(317 reference statements)

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“…Lipid accumulation is necessary but not sufficient for progression from simple steatosis to the more serious NAFLD; other insults are also required. For instance, overproduction of fatty acids accelerates hepatocyte death by promoting oxidative stress and mitochondrial dysfunction, which amplifies the inflammatory response intended to clear damaged hepatocytes ( 1 ). Hence, oxidative stress and inflammation are implicated in the development of advanced NAFLD.…”

Section: Discussionmentioning

confidence: 99%

“…The prevalence of nonalcoholic fatty liver is increasing worldwide as a result of an increasingly sedentary lifestyle and excess food intake. Although nonalcoholic fatty liver is considered not to cause serious liver damage, it can progress to nonalcoholic fatty liver disease (NAFLD), which involves nonalcoholic steatohepatitis, fibrosis, cirrhosis, and cancer ( 1 ). Because there are no approved drugs for advanced NAFLD, it must be appropriately managed at an early stage.…”

Section: Introductionmentioning

confidence: 99%

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Hemistepsin A inhibits T0901317-induced lipogenesis in the liver

et al. 2021

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Hemistepsin A (HsA) is a guaianolide sesquiterpene lactone that inhibits hepatitis and liver fibrosis. We evaluated the effects of HsA on liver X receptor (LXR)-mediated hepatic lipogenesis in vitro and in vivo . Up to 10 μM, HsA did not affect the viability of HepG2 and Huh7 cells. Pretreatment with 5-10 μM HsA significantly decreased the luciferase activity of the LXR response element, which was transactivated by T0901317, GW 3965, and LXRα/retinoid X receptor α overexpression. In addition, it significantly inhibited the mRNA expression of LXRα in HepG2 and Huh7 cells. It also suppressed the expression of sterol regulatory element-binding protein-1c and lipogenic genes and reduced the triglyceride accumulation triggered by T0901317. Intraperitoneal injection of HsA (5 and 10 mg/kg) in mice significantly alleviated the T0901317-mediated increases in hepatocyte diameter and the percentage of regions in hepatic parenchyma occupied by lipid droplets. Furthermore, HsA significantly attenuated hepatic triglyceride accumulation by restoring the impaired expression of LXRα-dependent lipogenic genes caused by T0901317. Therefore, based on its inhibition of the LXRα-dependent signaling pathway, HsA has prophylactic potential for steatosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hemistepsin A inhibits T0901317-induced lipogenesis in the liver

et al. 2021

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“…This is achieved via fusion of lysosomes with the plasma membrane. [90][91][92] Lysosomal exocytosis is an important function that any cell type performs. 93 Upon release, the content of lysosomes travels through the extracellular fluid for varying times and distances and subsequently interacts with recognized target cells to achieve the intercellular communication.…”

Section: Lysosomal Exocytosismentioning

confidence: 99%

“…Lipotoxic responses also affect LSECs, a type of non-parenchymal cell that are specifically involved in maintaining hepatic vascular tone and quiescence of hepatic stellate cells that are responsible for the fibrotic response. Upon treatment with oxidized lipids 89 or palmitic acid, 90 LSCEs directly or indirectly triggered the release of reactive oxygen species (ROS) production, 91 which influences mechanisms related to inflammation and fibrosis. 87 Increased hepatic fat accumulation has also been associated with reduced levels of high-density lipoproteins (HDL) and increased levels of total plasma cholesterol, low-density lipoproteins (LDL) and very lowdensity lipoprotein particles, 92 the latter being involved with hepatic lipid export.…”

Section: Lipo-and Glucotoxicitymentioning

confidence: 99%

“…126 While macrophages play a key role in the inflammatory response, hepatic stellate cells are the main drivers of the fibrotic response. 143 After a damaging insult, stellate cells are activated, thereby secreting collagens and related matrix proteins that lead to generation of scar tissue or fibrosis, 91,144 a pathological process also described in atherosclerosis. 145 Relevantly, Chu et al recently demonstrated that exposing hepatic stellate cells to fatty acids resulted in an increased secretion of CCL20, resulting in a switch from a quiescent to an activated hepatic stellate cell.…”

Section: Hepatic Inflammation and Fibrosismentioning

confidence: 99%

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The entanglement of plasma Cathepsin D and metabolic disturbances

Ding¹

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People interested in the research are advised to contact the author for the final version of the publication, or visit the DOI to the publisher's website.• The final author version and the galley proof are versions of the publication after peer review.• The final published version features the final layout of the paper including the volume, issue and page numbers. Link to publication General rightsCopyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal. ContentsChapter 1 General introduction 7 Chapter 2 Nonalcoholic fatty liver disease 35 Chapter 3 Myosteatosis in NAFLD patients correlates with 75 plasma cathepsin D Chapter 4 Plasma cathepsin D activity is negatively associated 91 with hepatic insulin sensitivity in overweight and obese humans Chapter 5 Plasma cathepsin D activity rather than levels 113 correlates with metabolic parameters of type 2 diabetes in male individuals Chapter 6 Insulin resistance is possitively associated with plasma cathepsin D activity in NAFLD patients

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Research progress and application of liver organoids for disease modeling and regenerative therapy

Hu,

Geng,

Wang

et al. 2024

J Mol Med

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The liver is a major metabolic organ of the human body and has a high incidence of diseases. In recent years, the annual incidence of liver disease has increased, seriously endangering human life and health. The study of the occurrence and development mechanism of liver diseases, discovery of new therapeutic targets, and establishment of new methods of medical treatment are major issues related to the national economy and people’s livelihood. The development of stable and effective research models is expected to provide new insights into the pathogenesis of liver diseases and the search for more effective treatment options. Organoid technology is a new in vitro culture system, and organoids constructed by human cells can simulate the morphological structure, gene expression, and glucose and lipid metabolism of organs in vivo, providing a new model for related research on liver diseases. This paper reviews the latest research progress on liver organoids from the establishment of cell sources and application of liver organoids and discusses their application potential in the field of liver disease research.

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Nonalcoholic Fatty Liver Disease

Cited by 10 publications

References 307 publications

Hemistepsin A inhibits T0901317-induced lipogenesis in the liver

Hemistepsin A inhibits T0901317-induced lipogenesis in the liver

The entanglement of plasma Cathepsin D and metabolic disturbances

Research progress and application of liver organoids for disease modeling and regenerative therapy

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