Burden of liver diseases in the world

Asrani, Sumeet K.; Devarbhavi, Harshad; Eaton, John E.; Kamath, Patrick S.

doi:10.1016/j.jhep.2018.09.014

Cited by 2,683 publications

(2,051 citation statements)

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“…Globally, liver cirrhosis ranks 11th in the most common causes of adult deaths, and nearly one million people die of liver cirrhosis annually (Asrani, Devarbhavi, Eaton, & Kamath, ). In most developed countries, liver cirrhosis is mainly caused by the hepatitis C virus and alcohol abuse, while non‐alcoholic livers will gradually increase (Tsochatzis, Bosch, & Burroughs, ).…”

Section: Introductionmentioning

confidence: 99%

Decellularized liver matrix as substrates for rescue of acute hepatocytes toxicity

2019

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More and more scholars regard the lesion of liver cirrhosis as a series of progressive clinical stages. Besides, liver cirrhosis is a late stage of scarring (fibrosis) of the liver, and has long been a common cause of death for the global adult population, thus, the treatment of liver cirrhosis is a key point investigated in the biomedical field. Here, we propose a novel hypothesis; if decellularized liver matrix (DLM) is possible injected into the injurant‐induced fiberized liver via the hepatic portal vein to thoroughly repair the liver, it may be an effective therapeutic method for liver fibrosis or even liver cirrhosis. This study mixed rat DLM with gelatin‐hydroxyphenylpropionic acid (Glt‐HPA) to form a three‐dimensional structure to simulate the in vivo liver environment, and cultured the primary rat hepatocytes in it. Afterward, the hepatocytes were treated using D‐galactosamine (GaIN), CHCl3, and CCl4‐containing medium to simulate the toxin‐mediated liver fibrosis in vitro. Finally, they were cultured in a DLM‐containing medium to observe the viability and functions of the damaged hepatocytes, and the hypothesis of this research was proved, meaning that Glt‐HPA‐DLM acting on damaged hepatocytes may repair them. Results have shown that Glt‐HPA‐DLM was effective for hepatocytes culture and repaired injured hepatocytes from GaIN, CHCl3, and CCl4 (albumin synthesis was increased by 219, 108, and 12%, respectively, whereas relative lactate dehydrogenase activity was reduced by 38, 68, and 67%, after 5 days of culture, separately). This research shows promising effects against hepatic fibrosis and may have potential for liver cirrhosis in vivo.

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Section: Introductionmentioning

confidence: 99%

Decellularized liver matrix as substrates for rescue of acute hepatocytes toxicity

2019

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“…Nonalcoholic fatty liver disease (NAFLD) is characterized by the presence of hepatic steatosis in the absence of any secondary causes of excessive accumulation of fat, such as excessive alcohol drinking (1). The current prevalence of NAFLD is 80% in patients with obesity and 30% in healthy individuals in general Western populations, and it has become the leading causes of chronic liver damage in Western countries (2). Approximately 15‐25% of patients with NAFLD develop nonalcoholic steatohepatitis, which may progress to more serious diseases such as liver cirrhosis and hepatocellular carcinoma (3, 4).…”

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confidence: 99%

Long‐term exercise prevents hepatic steatosis: a novel role of FABP1 in regulation of autophagy‐lysosomal machinery

Pi¹,

Liu²,

Chen³

et al. 2019

The FASEB Journal

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Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent diseases worldwide. Exercise is a first‐line therapy and an important preventive measure for patients with NAFLD, but the underlying mechanisms are not clear. C57BL/6 mice were fed a high‐fat diet (HFD) and subjected to 12 wk swimming exercise. Exercise protected against hepatic lipid accumulation and alleviated hepatocyte damage in HFD mice. Tandem mass tag—based quantitative proteomic analyses and ingenuity pathway analysis revealed that exercise down‐regulated fatty acid‐binding protein (FABP) 1 signaling pathway, which was most closely associated with lipid metabolism. Moreover, exercise significantly decreased FABP1 expression, and liver‐specific overexpression of FABP1 abolished the protective effect of exercise in NAFLD mice. Specifically, exercise significantly increased autophagic flux via restoring lysosomal function, including lysosomal proteolysis and lysosomal acidification maintenance, contributing to enhancement in autophagic clearance and subsequently alleviation of hepatic steatosis. Conversely, Fabp1 overexpression in the mouse liver blocked the protective effect of exercise via inhibiting autophagy flux. The present study identified FABP1 inhibition‐mediated replenishment of the autophagy‐lysosomal machinery as a novel endogenous mechanism whereby long‐term exercise improves lipid homeostasis and ameliorates hepatic steatosis in NAFLD.—Pi, H., Liu, M., Xi, Y., Chen, M., Tian, L., Xie, J., Chen, M., Wang, Z., Yang M., Yu, Z., Zhou, Z., Gao, F. Long‐term exercise prevents hepatic steatosis: a novel role of FABP1 in regulation of autophagy‐lysosomal machinery. FASEB J. 33, 11870‐11883 (2019). http://www.fasebj.org

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“…Not surprisingly, patients with decompensated disease have high rates of rehospitalization with admission costs estimated at $25,000 (1) and approximately one third of patients receiving guideline-concordant cirrhosis management. (2) The reasons for gaps in care and resulting high acute care utilization are multifactorial, including the complexity of the patient population and challenges with care delivery. With an expected increase in the number of patients with cirrhosis, our traditional model of primary care and gastroenterology/hepatology-based care delivery deserves closer evaluation.…”

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confidence: 99%

“…In addition to the clinical complications related to hepatic dysfunction and portal hypertension, patients contend with extensive comorbidities, physical frailty, psychosocial factors, addictions, and the challenge of navigating through a web of often disconnected provider appointments and tests. Not surprisingly, patients with decompensated disease have high rates of rehospitalization with admission costs estimated at $25,000 and approximately one third of patients receiving guideline‐concordant cirrhosis management . The reasons for gaps in care and resulting high acute care utilization are multifactorial, including the complexity of the patient population and challenges with care delivery.…”

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confidence: 99%

Advanced Practice Providers: Raising Our Defenses Against the Rising Tide of Cirrhosis

et al. 2020

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Burden of liver diseases in the world

Cited by 2,683 publications

References 210 publications

Decellularized liver matrix as substrates for rescue of acute hepatocytes toxicity

Decellularized liver matrix as substrates for rescue of acute hepatocytes toxicity

Long‐term exercise prevents hepatic steatosis: a novel role of FABP1 in regulation of autophagy‐lysosomal machinery

Advanced Practice Providers: Raising Our Defenses Against the Rising Tide of Cirrhosis

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