Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention

Younossi, Zobair M.; Anstee, Quentin M.; Marietti, Milena; Hardy, Timothy; Henry, Linda; Eslam, Mohammed; George, Jacob; Bugianesi, Elisabetta

doi:10.1038/nrgastro.2017.109

Cited by 4,161 publications

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References 114 publications

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“…Nonalcoholic steatohepatitis (NASH) is one of the most common chronic liver diseases. The incidence and prevalence of NASH is on the rise in parallel with increasing obesity and metabolic syndrome . NASH is characterized by the presence of hepatic steatosis, inflammation, and evidence of hepatocellular damage.…”

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confidence: 99%

Sestrin 3 Protects Against Diet‐Induced Nonalcoholic Steatohepatitis in Mice Through Suppression of Transforming Growth Factor β Signal Transduction

et al. 2019

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Sestrin 3 (Sesn3) belongs to the three‐member sestrin protein family. Sestrins have been implicated in antioxidative stress, adenosine monophosphate–activated protein kinase and mammalian target of rapamycin signal transduction, and metabolic homeostasis. However, the role of Sesn3 in the development of nonalcoholic steatohepatitis (NASH) has not been previously studied. In this work, we generated Sesn3 whole‐body knockout and liver‐specific transgenic mice to investigate the hepatic function of Sesn3 in diet‐induced NASH. With only 4 weeks of dietary treatment, Sesn3 knockout mice developed severe NASH phenotype as characterized by hepatic steatosis, inflammation, and fibrosis. Strikingly, after 8‐week feeding with a NASH‐inducing diet, Sesn3 transgenic mice were largely protected against NASH development. Transcriptomic analysis revealed that multiple extracellular matrix–related processes were up‐regulated, including transforming growth factor β (TGF‐β) signaling and collagen production. Further biochemical and cell biological analyses have illustrated a critical control of the TGF‐β–mothers against decapentaplegic homolog (Smad) pathway by Sesn3 at the TGF‐β receptor and Smad3 levels. First, Sesn3 inhibits the TGF‐β receptor through an interaction with Smad7; second, Sesn3 directly inhibits the Smad3 function through protein–protein interaction and cytosolic retention. Conclusion: Sesn3 is a critical regulator of the extracellular matrix and hepatic fibrosis by suppression of TGF‐β–Smad3 signaling.

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confidence: 99%

Sestrin 3 Protects Against Diet‐Induced Nonalcoholic Steatohepatitis in Mice Through Suppression of Transforming Growth Factor β Signal Transduction

et al. 2019

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“…Nonalcoholic fatty liver disease (NAFLD) has become one of the main causes of chronic liver diseases, with an estimated global prevalence of 25%‐30%, rising up to 90% in morbidly obese patients . NAFLD includes simple steatosis (SS) and nonalcoholic steatohepatitis (NASH), which may advance to cirrhosis and hepatocellular carcinoma (HCC) .…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori infection and nonalcoholic fatty liver disease: Time for large clinical trials evaluating eradication therapy

Polyzos

2019

Helicobacter

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“…Among these diseases, NAFLD is one of the most prevalent chronic liver diseases and is an emerging global public health threat. NAFLD affects about 1.8 billion people worldwide with a prevalence of ~20–30% (1). The pathological spectrum of NAFLD ranges from simple steatosis to advanced stages including non-alcoholic steatohepatitis (NASH), hepatic fibrosis, and cirrhosis.…”

Section: Introductionmentioning

confidence: 99%

“…The prevalence of simple steatosis with lipid accumulation exceeding 5% of liver weight ranges from 15 to 40% in the general population. Among patients with simple steatosis, 10–20% develop NASH which is defined as steatosis with hepatic inflammation and fibrosis (1). NASH can progress to more severe stages such as cirrhosis and HCC (2).…”

Section: Introductionmentioning

confidence: 99%

Pathogenesis of Nonalcoholic Steatohepatitis and Hormone-Based Therapeutic Approaches

Kim

Lee

2018

Front. Endocrinol.

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Non-alcoholic fatty liver disease (NAFLD) is an emerging global health problem and a potential risk factor for type 2 diabetes, cardiovascular disease, and chronic kidney disease. Nonalcoholic steatohepatitis (NASH), an advanced form of NAFLD, is a predisposing factor for development of cirrhosis and hepatocellular carcinoma. The increasing prevalence of NASH emphasizes the need for novel therapeutic approaches. Although therapeutic drugs against NASH are not yet available, fundamental insights into the pathogenesis of NASH have been made during the past few decades. Multiple therapeutic strategies have been developed and are currently being explored in clinical trials or preclinical testing. The pathogenesis of NASH involves multiple intracellular/extracellular events in various cell types in the liver or crosstalk events between the liver and other organs. Here, we review current findings and knowledge regarding the pathogenesis of NASH, focusing on the most recent advances. We also highlight hormone-based therapeutic approaches for treatment of NASH.

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Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention

Cited by 4,161 publications

References 114 publications

Sestrin 3 Protects Against Diet‐Induced Nonalcoholic Steatohepatitis in Mice Through Suppression of Transforming Growth Factor β Signal Transduction

Sestrin 3 Protects Against Diet‐Induced Nonalcoholic Steatohepatitis in Mice Through Suppression of Transforming Growth Factor β Signal Transduction

Helicobacter pylori infection and nonalcoholic fatty liver disease: Time for large clinical trials evaluating eradication therapy

Pathogenesis of Nonalcoholic Steatohepatitis and Hormone-Based Therapeutic Approaches

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