Global epidemiology of non‐alcoholic fatty liver disease/non‐alcoholic steatohepatitis: What we need in the future

Araújo, Ana Ruth; Rosso, Natalia; Bedogni, Giorgio; Tiribelli, Claudio; Bellentani, Stefano

doi:10.1111/liv.13643

Cited by 340 publications

(280 citation statements)

References 35 publications

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“…Patients with NASH have additional risk factors for thrombosis. NASH is correlated with obesity . Obesity is associated with increased levels of plasminogen activator inhibitor‐1 .…”

Section: Clinical Context Of Iri In Liver Transplantationmentioning

confidence: 99%

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Dar

Sullivan

Bynon

et al. 2019

Liver International

261

245

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Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia‐reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll‐like receptor signalling, alterations in micro‐RNA expression, production of ROS, regulation of autophagy and activation of hypoxia‐inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation – a process that will lead to improved outcomes for patients suffering from end‐stage liver disease.

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“…Patients with NASH have additional risk factors for thrombosis. NASH is correlated with obesity . Obesity is associated with increased levels of plasminogen activator inhibitor‐1 .…”

Section: Clinical Context Of Iri In Liver Transplantationmentioning

confidence: 99%

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Dar

Sullivan

Bynon

et al. 2019

Liver International

261

245

View full text Add to dashboard Cite

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“…It is now considered to be a key hepatic manifestation of metabolic syndrome (MetS) . The global prevalence of NAFLD is 25% . The estimated overall prevalence of NAFLD in Asia is steadily increasing and was recently reported to be around 27% .…”

Section: Introductionmentioning

confidence: 99%

Association of metabolic syndrome and patatin‐like phospholipase 3 – rs738409 gene variant in non‐alcoholic fatty liver disease among a Chennai‐based south Indian population

Narayanasamy

Rajendran

Panneerselvam

et al. 2020

The Journal of Gene Medicine

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Background Non‐alcoholic fatty liver disease (NAFLD) is commonly diagnosed in patients presenting with metabolic syndrome (MetS) and has been associated with single nucleotide polymorphisms of rs738409 in the patatin‐like phospholipase domain containing 3 (PNPLA3) gene. This association remains to be investigated in the South Indian population. We aimed to determine the association of the PNPLA3 rs738409 gene polymorphism with MetS and NAFLD among a Chennai‐based population. Methods The study comprised 105 NAFLD cases and 102 controls. All subjects were genotyped for the PNPLA3 rs738409 variant and MetS was defined according to the National Cholesterol Education Program – Adult Treatment Panel III criteria. Our case–control study showed the association of the variant with NAFLD and MetS. Results The PNPLA3 rs738409 variant was associated with NAFLD and the genotype frequencies (CC/CG/GG) were 19 (18.1%), 50 (47.6%) and 36 (34.3%) in the NAFLD group and 59 (57.8%), 29 (28.4%) and 14 (13.7%) in the control group respectively. We also confirmed the interaction between the PNPLA3 rs738409 polymorphism and MetS with respect tto elevated triglyceride levels. However, an association with elevated waist circumference, fasting glucose, blood pressure and decreased high‐density lipoprotein cholesterol was not observed in the present study. Conclusions The PNPLA3 rs738409 gene polymorphism increases the risk of NAFLD by up to four‐fold in subjects with an elevated level of triglyceride independent of other features of MetS.

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“…Liver cancer is the second leading cause of cancer‐related death worldwide, and hepatocellular carcinoma (HCC) comprises approximately 80% of liver cancer cases . While the predominant cause of liver cancer, hepatitis virus infection, has been decreasing sharply with the advent of novel antiviral drugs, other causes, such as non‐alcoholic fatty liver disease and non‐alcoholic steatohepatitis, have been increasing, especially in developed countries . Given the poor prognosis of liver cancer, development of innovative therapies for HCC is strongly desired.…”

Section: Introductionmentioning

confidence: 99%

Prolonged inhibition of hepatocellular carcinoma cell proliferation by combinatorial expression of defined transcription factors

et al. 2018

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Hepatocellular carcinoma (HCC) accounts for a large proportion of liver cancer cases and has an extremely poor prognosis. Therefore, novel innovative therapies for HCC are strongly desired. As gene therapy tools for HCC, 2 hepatic transcription factors (TF), HNF4A and HNF1A, have been used to suppress proliferation and to extinguish cancer‐specific characteristics of target cells. However, our present data demonstrated that single transduction of HNF4A or HNF1A had only a limited effect on suppression of HCC cell proliferation. Thus, in this study, we examined whether combinations of TF could show more effective antitumor activity, and found that combinatorial transduction of 3 hepatic TF, HNF4A, HNF1A and FOXA3, suppressed HCC cell proliferation more stably than single transduction of these TF. The combinatorial transduction also suppressed cancer‐specific phenotypes, such as anchorage‐independent growth in culture and tumorigenicity after transplantation into mice. HCC cell lines transduced with the 3 TF did not recover their proliferative property after withdrawal of anticancer drugs, indicating that combinatorial expression of the 3 TF suppressed the growth of all cell subtypes within the HCC cell lines, including cancer stem‐like cells. Transcriptome analyses revealed that the expression levels of a specific gene set involved in cell proliferation were only decreased in HCC cells overexpressing all 3 TF. Moreover, combined transduction of the 3 TF could facilitate hepatic differentiation of HCC cell lines. Our strategy for inducing stable inhibition and functional differentiation of tumor cells using a defined set of TF will become an effective therapeutic strategy for various types of cancers.

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Global epidemiology of non‐alcoholic fatty liver disease/non‐alcoholic steatohepatitis: What we need in the future

Cited by 340 publications

References 35 publications

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Association of metabolic syndrome and patatin‐like phospholipase 3 – rs738409 gene variant in non‐alcoholic fatty liver disease among a Chennai‐based south Indian population

Prolonged inhibition of hepatocellular carcinoma cell proliferation by combinatorial expression of defined transcription factors

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