Advancing the understanding of NAFLD to hepatocellular carcinoma development: From experimental models to humans

Chen, Kan; Ma, Jianbo; Jia, Xiaoyuan; Ai, Wen; Ma, Zhiyong; Pan, Qiuwei

doi:10.1016/j.bbcan.2018.11.005

Cited by 60 publications

(48 citation statements)

References 130 publications

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“…Indeed, it has been previously shown that circadian rhythm is driving oscillations in hepatic triglyceride levels, inflammation, oxidative stress, mitochondrial dysfunction, and hepatic insulin resistance [107,108]. Moreover, it has been recently suggested that chronic disruption of circadian rhythm may spontaneously induce the progression from NAFLD to NASH, fibrosis, and HCC [20,109], similar to the human situation, pointing towards its translational value.…”

Section: Other Murine Modelsmentioning

confidence: 99%

“…One of the simplest ways of disturbing lipid metabolism, inducing steatosis and moderate NASH, is by the administration of a regular high-fat diet (HFD; 60% fat, 20% proteins, 20% carbohydrates) [18,19]. For instance, feeding wild-type C57BL/6 mice a HFD for 10-12 weeks resulted in phenotypic changes such as hyperlipidemia, hyperinsulinemia, and glucose intolerance [19,20]. Despite hepatic steatosis, inflammatory cell infiltration was not present until 19 weeks of HFD intake [19].…”

Section: Dietary Murine Modelsmentioning

confidence: 99%

“…To overcome the lack of severe hepatic fibrosis often observed in preclinical models, mice are commonly fed MCD [47] or a diet low in/deficient for choline (CD) [48]. Although CD exacerbated fatty liver [48], MCD resulted in rapid NASH development with severe liver fibrosis within 4-10 weeks, likely as a consequence of reduced VLDL synthesis and hepatic-β oxidation [20]. While liver inflammation and elevated circulating liver enzyme levels returned back to normal levels after switching the diet back to control within 16 weeks, fibrosis and CD68-positive macrophages remained present [47].…”

Section: Dietary Murine Modelsmentioning

confidence: 99%

“…Another well-known model is based on a knock-in of the Patatin-like phospholipase domain-containing 3 (PNPLA3) polymorphism [20], which was found to be present in approximately one-fifth of our population [69,70]. PNPLA3 is a functional enzyme with acyltransferase and/or lipase activity towards phospholipids and/or triglycerides and retinyl esters, respectively [71].…”

Section: Genetic Murine Modelsmentioning

confidence: 99%

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NAFLD Preclinical Models: More than a Handful, Less of a Concern?

Oligschlaeger

Shiri-Sverdlov

2020

Biomedicines

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Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver diseases ranging from simple steatosis to non-alcoholic steatohepatitis, fibrosis, cirrhosis, and/or hepatocellular carcinoma. Due to its increasing prevalence, NAFLD is currently a major public health concern. Although a wide variety of preclinical models have contributed to better understanding the pathophysiology of NAFLD, it is not always obvious which model is best suitable for addressing a specific research question. This review provides insights into currently existing models, mainly focusing on murine models, which is of great importance to aid in the identification of novel therapeutic options for human NAFLD.

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Section: Other Murine Modelsmentioning

confidence: 99%

Section: Dietary Murine Modelsmentioning

confidence: 99%

Section: Dietary Murine Modelsmentioning

confidence: 99%

Section: Genetic Murine Modelsmentioning

confidence: 99%

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NAFLD Preclinical Models: More than a Handful, Less of a Concern?

Oligschlaeger

Shiri-Sverdlov

2020

Biomedicines

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“…Similar results were reported by a Japanese study, in which 49% of NAFLD associated HCC cases arose without cirrhosis [33] , and a German study where 41.7% of the cases arose without cirrhosis [34] . Furthermore, in animal models, diet-induced NAFLD leads to spontaneous HCC [35] .…”

Section: Nafld Increases the Risk Of Liver Cancermentioning

confidence: 99%

Molecular links between non-alcoholic fatty liver disease and hepatocellular carcinoma

Raza¹,

Rajak²,

Anjum³

et al. 2019

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Non-alcoholic fatty liver disease (NAFLD) and its advanced complication, non-alcoholic steatohepatitis (NASH), have become leading causes of hepatocellular carcinoma (HCC) worldwide. In this review, we discuss the role of metabolic, gut microbial, immune and endocrine mediators which promote the progression of NAFLD to HCC. In particular, this progression involves multiple hits resulting from lipotoxicity, oxidative stress, inhibition of hepatic autophagy and inflammation. Furthermore, dysbiosis in the gut associated with obesity also promotes HCC via induction of proinflammatory cytokines and Toll like receptor signalling as well as altered bile metabolism. Additionally, compromised T-cell function and impaired hepatic hormonal action promote the development of NASH-associated HCC. Lastly, we discuss the current challenges involved in the diagnosis and treatment of NAFLD/NASH-associated HCC.

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Non-alcoholic Fatty Liver Disease

Kim,

Choi

2023

Metabolic Syndrome

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Advancing the understanding of NAFLD to hepatocellular carcinoma development: From experimental models to humans

Cited by 60 publications

References 130 publications

NAFLD Preclinical Models: More than a Handful, Less of a Concern?

NAFLD Preclinical Models: More than a Handful, Less of a Concern?

Molecular links between non-alcoholic fatty liver disease and hepatocellular carcinoma

Non-alcoholic Fatty Liver Disease

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