Biology of Liver Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1569

Special Issue Editors


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Guest Editor
Department of Gastroenterology, Nara Medical University, 840 Shijo-cho, Kashihara 634-8522, Nara, Japan
Interests: liver fibrosis; diabetes mellitus; inflammation; steatosis
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Gastroenterology, Nara Medical University, Kashihara 634-8522, Nara, Japan
Interests: gastroenterology; liver cirrhosis; acute liver failure; hepatocellular carcinoma, ADAMTS13, von Willebrand factor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Research into liver diseases such as viral hepatitis, liver cirrhosis and hepatocellular carcinoma has made significant progress in recent years. However, it is still insufficient, and liver disease remains a leading cause of death. Further advances in liver disease research are needed to reduce deaths from liver disease.

For example, sarcopenia, the gut–liver axis and blood coagulation have recently been reported to be associated with the pathophysiology of liver disease. Thus, we believe that further research on liver disease will provide new insights.

In this Special Issue entitled “Biology of Liver Diseases”, we invite a wide range of papers, including basic research, clinical research, and review articles. We look forward to receiving high-quality papers from relevant researchers.

Dr. Tadashi Namisaki
Dr. Hiroaki Takaya
Guest Editors

Manuscript Submission Information

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Keywords

  • viral hepatitis
  • alcoholic hepatitis
  • non-alcoholic steatohepatitis
  • autoimmune hepatitis
  • primary biliary cholangitis
  • liver cirrhosis
  • liver cancer
  • portal hypertension

Published Papers (1 paper)

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Research

14 pages, 5945 KiB  
Article
A New Non-Obese Steatohepatitis Mouse Model with Cardiac Dysfunction Induced by Addition of Ethanol to a High-Fat/High-Cholesterol Diet
by Seiji Shiraishi, Jinyao Liu, Yuki Saito, Yumiko Oba, Yuiko Nishihara and Satomichi Yoshimura
Biology 2024, 13(2), 91; https://doi.org/10.3390/biology13020091 - 1 Feb 2024
Viewed by 1273
Abstract
Non-obese metabolic dysfunction-associated steatotic liver disease (MASLD) has been associated with cardiovascular-related mortality, leading to a higher mortality rate compared to the general population. However, few reports have examined cardiovascular events in non-obese MASLD mouse models. In this study we created a mouse [...] Read more.
Non-obese metabolic dysfunction-associated steatotic liver disease (MASLD) has been associated with cardiovascular-related mortality, leading to a higher mortality rate compared to the general population. However, few reports have examined cardiovascular events in non-obese MASLD mouse models. In this study we created a mouse model to mimic this condition. In this study involving seven-week-old C57BL/6J male mice, two dietary conditions were tested: a standard high-fat/high-cholesterol diet (STHD-01) and a combined diet of STHD-01 and ethanol. Over periods of 6 and 12 weeks, we analyzed the effects on liver and cardiac tissues using various staining techniques and PCR. Echocardiography and blood tests were also performed to assess cardiac function and liver damage. The results showed that mice on the ethanol-supplemented STHD-01 diet developed signs of steatohepatitis and cardiac dysfunction, along with increased sympathetic activity, as early as 6 weeks. At 12 weeks, more pronounced exacerbations accompanied with cardiac dilation, advanced liver fibrosis, and activated myocardial fibrosis with sympathetic activation were observed. This mouse model effectively replicated non-obese MASLD and cardiac dysfunction over a 12-week period using a combined diet of STHD-01 and ethanol. This dietary approach highlighted that both liver inflammation and fibrosis, as well as cardiac dysfunction, could be significantly worsened due to the activation of the sympathetic nervous system. Our results indicate that alcohol, even when completely metabolized on the day of drinking, exacerbates the progression of non-obese MASLD and cardiac dysfunction. Full article
(This article belongs to the Special Issue Biology of Liver Diseases)
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