Nonalcoholic steatohepatitis

Bzowej, Natalie

doi:10.1097/mot.0000000000000502

Cited by 30 publications

(11 citation statements)

References 42 publications

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“…Furthermore, approximately 25% NAFLD patients can progress to NASH and up to a third of these have NASH [2]. NASH is a serious liver disease that can further progress to cirrhosis, hepatocellular cancer, and liver failure and is projected to become the leading cause of liver transplantation in the next several years, particularly since, currently, there are no approved therapeutic strategies for NAFLD/NASH [3].…”

Section: Introductionmentioning

confidence: 99%

“…The results from both the pre-clinical and clinical trials distinctly point to a combinatorial approach (lipid regulation, anti-inflammatory, antioxidant, and anti-fibrosis) as a therapeutic remedy for NASH. Nowadays, the absence of approved pharmacological therapies for NASH is a primary incentive for research into developing new potent candidates for this condition [3].…”

Section: Introductionmentioning

confidence: 99%

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2, 3, 4′, 5-tetrahydroxystilbene-2-0-β-d Glycoside Attenuates Age- and Diet-Associated Non-Alcoholic Steatohepatitis and Atherosclerosis in LDL Receptor Knockout Mice and Its Possible Mechanisms

Peng

Zhang

et al. 2019

IJMS

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The compound, 2,3,5,4′-tetrahydroxystilbene-2-O-β-d-glucoside (TSG), a primary bioactive polyphenolic component of Polygonum multiflorum exerts numerous pharmacological activities. However, its protective effect against non-alcoholic steatohepatitis (NASH), in the context of metabolic syndrome, remains poorly understood. The aim of the present study is to evaluate the effects of TSG treatment on middle-aged (12-mo-old) male LDLr−/− mice, which were fed a high fat diet for 12 weeks to induce metabolic syndrome and NASH. At the end of the experiment, the blood samples of mice were collected for determination of metabolic parameters. Liver and aorta tissues were collected for analysis, such as histology, immunofluorescence, hepatic lipid content, real-time PCR, and western blot. Our data show that TSG treatment improved the different aspects of NASH (steatosis, inflammation, and fibrosis) and atherosclerosis, as well as some of the metabolic basal characteristics. These modulatory effects of TSG are mediated, at least in part, through regulating key regulators of lipid metabolism (SREBP1c, PPARα and their target genes, ABCG5 and CYP7A1), inflammation (CD68, TNF-α, IL-6 and ICAM), fibrosis (α-SMA and TNFβ) and oxidative stress (NADPH-oxidase 2/4, CYP2E1 and antioxidant enzymes). These results suggest that TSG may be a promising candidate for preventing and treating the progression of NASH.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

2, 3, 4′, 5-tetrahydroxystilbene-2-0-β-d Glycoside Attenuates Age- and Diet-Associated Non-Alcoholic Steatohepatitis and Atherosclerosis in LDL Receptor Knockout Mice and Its Possible Mechanisms

Peng

Zhang

et al. 2019

IJMS

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“…NASH is projected to become the most common indication for liver transplantation in near future[ 73 ]. With the availability of highly effective treatment options for hepatitis C virus (HCV)-related cirrhosis, NASH-related cirrhosis is emerging as the leading indication for liver transplantation worldwide.…”

Section: Available Treatment Options For Nonalcoholic Fatty Liver Andmentioning

confidence: 99%

“…Being a complex procedure, liver transplantation is associated with several limitations. Another important aspect to consider is that liver transplantation does not treat the comorbidities of NASH and therefore interventions to address the accompanying metabolic diseases is important, before and after transplantation[ 73 ].…”

Section: Available Treatment Options For Nonalcoholic Fatty Liver Andmentioning

confidence: 99%

Management of nonalcoholic fatty liver disease in the Middle East

Sanai

Abaalkhail

Hasan

et al. 2020

WJG

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The prevalence of nonalcoholic fatty liver disease (NAFLD) in the Middle East is increasing in parallel to an increase in the prevalence of associated risk factors such as obesity, metabolic syndrome, and type 2 diabetes mellitus. About 20% to 30% of the patients progress to develop nonalcoholic steatohepatitis (NASH), a histological subtype of NAFLD, with features of hepatocyte injury such as hepatocyte ballooning. NASH can progress to fibrosis, cirrhosis, and even hepatocellular carcinoma. NAFLD thus causes a substantial burden on healthcare systems and it is imperative that appropriate strategies are discussed at a regional level to facilitate effective management tailored to the needs of the region. To fulfil this unmet need, expert gastroenterologists, hepatologists, and endocrinologists from the region came together in three advisory board meetings that were conducted in Saudi Arabia, United Arab Emirates, and Kuwait, to discuss current local challenges in NAFLD screening and diagnosis, and the different available management options. The experts discussed the disease burden of NAFLD/NASH in the Middle East; screening, diagnosis, and referral patterns in NAFLD; and available treatment options for NAFLD and NASH. This paper summarizes the discussions and opinion of the expert panel on the management of NAFLD/NASH and also presents an extensive literature review on the topic.

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“…Nonalcoholic fatty liver disease (NAFLD) is a chronic and progressive liver disease which is evolving to be one of the leading causes for liver transplantation [ 1 – 3 ]. As the most common chronic liver disease in Western countries, NAFLD is accompanied by a specific sequence of hepatic alterations that begins with simple steatosis which can easily progress to more advanced stages like nonalcoholic steatohepatitis (NASH), liver fibrosis, and cirrhosis and finally the development of hepatocellular carcinoma (HCC) leading to an increased mortality [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

c‐Met Signaling Protects from Nonalcoholic Steatohepatitis‐ (NASH‐) Induced Fibrosis in Different Liver Cell Types

Drescher

Schumacher

Schenker

et al. 2018

Oxidative Medicine and Cellular Longevity

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Nonalcoholic steatohepatitis (NASH) is the most common chronic, progressive liver disease in Western countries. The significance of cellular interactions of the HGF/c-Met axis in different liver cell subtypes and its relation to the oxidative stress response remains unclear so far. Hence, the present study is aimed at investigating the role of c-Met and the interaction with the oxidative stress response during NASH development in mice and humans. Conditional c-Met knockout (KO) lines (LysCre for Kupffer cells/macrophages, GFAPCre for α-SMA+ and CK19+ cells and MxCre for bone marrow-derived immune cells) were fed chow and either methionine-choline-deficient diet (MCD) for 4 weeks or high-fat diet (HFD) for 24 weeks. Mice lacking c-Met either in Kupffer cells, α-SMA+ and CK19+ cells, or bone marrow-derived immune cells displayed earlier and faster progressing steatohepatitis during dietary treatments. Severe fatty liver degeneration and histomorphological changes were accompanied by an increased infiltration of immune cells and a significant upregulation of inflammatory cytokine expression reflecting an earlier initiation of steatohepatitis development. In addition, animals with a cell-type-specific deletion of c-Met exhibited a strong generation of reactive oxygen species (ROS) by dihydroethidium (hydroethidine) (DHE) staining showing a significant increase in the oxidative stress response especially in LysCre/c-Metmut and MxCre/c-Metmut animals. All these changes finally lead to earlier and stronger fibrosis progression with strong accumulation of collagen within liver tissue of mice deficient for c-Met in different liver cell types. The HGF/c-Met signaling pathway prevents from steatosis development and has a protective function in the progression to steatohepatitis and fibrosis. It conveys an antifibrotic role independent on which cell type c-Met is missing (Kupffer cells/macrophages, α-SMA+ and CK19+ cells, or bone marrow-derived immune cells). These results highlight a global protective capacity of c-Met in NASH development and progression.

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Nonalcoholic steatohepatitis

Cited by 30 publications

References 42 publications

2, 3, 4′, 5-tetrahydroxystilbene-2-0-β-d Glycoside Attenuates Age- and Diet-Associated Non-Alcoholic Steatohepatitis and Atherosclerosis in LDL Receptor Knockout Mice and Its Possible Mechanisms

2, 3, 4′, 5-tetrahydroxystilbene-2-0-β-d Glycoside Attenuates Age- and Diet-Associated Non-Alcoholic Steatohepatitis and Atherosclerosis in LDL Receptor Knockout Mice and Its Possible Mechanisms

Management of nonalcoholic fatty liver disease in the Middle East

c‐Met Signaling Protects from Nonalcoholic Steatohepatitis‐ (NASH‐) Induced Fibrosis in Different Liver Cell Types

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