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Cellular and Molecular Pathogenesis of Hepatobiliary Diseases

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 21725

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Special Issue Editor

Dr. Jeongeun Hyun

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Guest Editor

Institute of Tissue Regeneration Engineering, Dankook University, Cheonan, Republic of Korea
Interests: nonalcoholic fatty liver disease (NAFLD); hepatobiliary cancer; liver cancer therapeutics

Special Issue Information

Dear Colleagues,

Hepatobiliary disease (HBD) occurs in the liver and biliary tract and is caused by various risk factors, such as infection, toxins, metabolic disorders, alcohol intake, and heart failure. Severe or chronic damage to the hepatobiliary system can result in tissue fibrosis, which can progress to cirrhosis and eventually lead to life-threatening conditions such as liver failure and hepatobiliary cancer. Hence, early intervention for HBD is important to prevent HBD from progressing to end-stage HBD. Although significant progress has been made in overcoming HBD through extensive research over the past few decades, it has also been revealed that the pathogenesis of HBD is complex and needs further investigation. This Special Issue will focus on understanding the cellular and molecular pathogenesis of HBD, which greatly contributes to the development of novel therapeutic strategies that are more specific and effective for the treatment of HBD patients. Authors are invited to submit original research or review articles related to this Special Issue.

Potential topics include but are not limited to:

Risk factors related to the development of HBD;
Novel cellular and molecular mechanisms of HBD pathogenesis;
Potential biomarkers for predicting the progression and response to therapy of HBD;
Currently available therapies for the treatment of HBD and future directions.

Dr. Jeongeun Hyun
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

alcoholic hepatitis
nonalcoholic steatohepatitis
hepatobiliary cancer
drug-induced hepatotoxicity
autoimmune liver disease
primary biliary cirrhosis
primary sclerosing cholangitis
gallbladder disease
cellular and molecular mechanisms of hepatobiliary disease
novel therapeutic strategies of hepatobiliary disease

Published Papers (5 papers)

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Research

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15 pages, 3412 KiB

Open AccessArticle

Peroxisome Proliferator-Activated Receptor α Has a Protective Effect on Fatty Liver Caused by Excessive Sucrose Intake

by Tomomi Yamazaki and Megumi Ihato

Biomedicines 2022, 10(9), 2199; https://doi.org/10.3390/biomedicines10092199 - 6 Sep 2022

Cited by 2 | Viewed by 1503

Abstract

Sterol regulatory element binding protein (SREBP)-1c is a transcription factor that regulates lipid synthesis from glucose in the liver. It is activated by sucrose, which activates the fatty acid synthesis pathway. On the other hand, peroxisome proliferator-activated receptor (PPAR) α regulates the transcription of several genes encoding enzymes involved in fatty acid β-oxidation in the liver. To evaluate the beneficial effects of PPARα on fatty liver caused by excessive sucrose intake, we investigated the molecular mechanisms related to the development of fatty liver in PPARα-deficient mice that were fed a high-sucrose diet (Suc). The SREBP-1c target gene expression was increased by sucrose intake, leading to the development of fatty liver. Furthermore, PPARα^−/− mice developed severe fatty liver. Male and female PPARα^−/− mice fed Suc showed 3.7- and 3.1-fold higher liver fat content than Suc-fed male and female wild-type mice, respectively. Thus, PPARα may work to prevent the development of fatty liver caused by excessive sucrose intake. Liver TG accumulation differed between male and female PPARα^−/− mice. A possible explanation is that male mice show the increased expression of Pparγ, which usually contributes to triglyceride synthesis in the liver, to compensate for Pparα deficiency. In contrast, female wild-type mice inherently have low Pparα levels. Thus, Pparα deficiency has less pronounced effects in female mice. A diet that activates PPARα may be effective for preventing the development of fatty liver due to excessive sucrose intake. Full article

(This article belongs to the Special Issue Cellular and Molecular Pathogenesis of Hepatobiliary Diseases)

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Review

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21 pages, 440 KiB

Open AccessReview

by Yoonji Ha, Inju Jeong and Tae Hyun Kim

Biomedicines 2022, 10(10), 2530; https://doi.org/10.3390/biomedicines10102530 - 10 Oct 2022

Cited by 10 | Viewed by 2476

Abstract

Alcohol-related liver disease (ALD) refers to a spectrum of liver manifestations ranging from fatty liver diseases, steatohepatitis, and fibrosis/cirrhosis with chronic inflammation primarily due to excessive alcohol use. Currently, ALD is considered as one of the most prevalent causes of liver disease-associated mortality worldwide. Although the pathogenesis of ALD has been intensively investigated, the present understanding of its biomarkers in the context of early clinical diagnosis is not complete, and novel therapeutic targets that can significantly alleviate advanced forms of ALD are limited. While alcohol abstinence remains the primary therapeutic intervention for managing ALD, there are currently no approved medications for treating ALD. Furthermore, given the similarities and the differences between ALD and non-alcoholic fatty liver disease in terms of disease progression and underlying molecular mechanisms, numerous studies have demonstrated that many therapeutic interventions targeting several signaling pathways, including oxidative stress, inflammatory response, hormonal regulation, and hepatocyte death play a significant role in ALD treatment. Therefore, in this review, we summarized several key molecular targets and their modes of action in ALD progression. We also described the updated therapeutic options for ALD management with a particular emphasis on potentially novel signaling pathways. Full article

(This article belongs to the Special Issue Cellular and Molecular Pathogenesis of Hepatobiliary Diseases)

18 pages, 3173 KiB

Open AccessReview

Combined Hepatocellular-Cholangiocarcinoma: An Update on Pathology and Diagnostic Approach

by Joon Hyuk Choi and Jae Y. Ro

Biomedicines 2022, 10(8), 1826; https://doi.org/10.3390/biomedicines10081826 - 29 Jul 2022

Cited by 7 | Viewed by 2682

Abstract

Combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a rare primary liver carcinoma displaying both hepatocytic and cholangiocytic differentiation within the same tumor. Relative to classic hepatocellular carcinoma (HCC), cHCC-CCA has more aggressive behavior and a poorer prognosis. Though recent advances have improved our understanding of the biology underlying cHCC-CCAs, they remain diagnostically challenging for pathologists because of their morphologic and phenotypic diversity. Accurate diagnosis of cHCC-CCA is important for patient management and prognostication. Herein, we review recent updates on cHCC-CCA, focusing on tumor classification, pathology, and diagnostic approach. Full article

(This article belongs to the Special Issue Cellular and Molecular Pathogenesis of Hepatobiliary Diseases)

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16 pages, 1934 KiB

Open AccessReview

The Emerging Role of Branched-Chain Amino Acids in Liver Diseases

by Emily Kwun Kwan Lo, Felicianna, Jing-Hang Xu, Qiao Zhan, Zheng Zeng and Hani El-Nezami

Biomedicines 2022, 10(6), 1444; https://doi.org/10.3390/biomedicines10061444 - 18 Jun 2022

Cited by 25 | Viewed by 7347

Abstract

Chronic liver diseases pose a substantial health burden worldwide, with approximately two million deaths each year. Branched-chain amino acids (BCAAs)—valine, leucine, and isoleucine—are a group of essential amino acids that are essential for human health. Despite the necessity of a dietary intake of BCAA, emerging data indicate the undeniable correlation between elevated circulating BCAA levels and chronic liver diseases, including non-alcoholic fatty liver diseases (NAFLD), cirrhosis, and hepatocellular carcinoma (HCC). Moreover, circulatory BCAAs were positively associated with a higher cholesterol level, liver fat content, and insulin resistance (IR). However, BCAA supplementation was found to provide positive outcomes in cirrhosis and HCC patients. This review will attempt to address the contradictory claims found in the literature, with a special focus on BCAAs’ distribution, key signaling pathways, and the modulation of gut microbiota. This should provide a better understanding of BCAAs’ possible contribution to liver health. Full article

(This article belongs to the Special Issue Cellular and Molecular Pathogenesis of Hepatobiliary Diseases)

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30 pages, 997 KiB

Open AccessReview

Primary Biliary Cholangitis and Primary Sclerosing Cholangitis: Current Knowledge of Pathogenesis and Therapeutics

by Ji-Won Park, Jung-Hee Kim, Sung-Eun Kim, Jang Han Jung, Myoung-Kuk Jang, Sang-Hoon Park, Myung-Seok Lee, Hyoung-Su Kim, Ki Tae Suk and Dong Joon Kim

Biomedicines 2022, 10(6), 1288; https://doi.org/10.3390/biomedicines10061288 - 31 May 2022

Cited by 21 | Viewed by 6906

Abstract

Cholangiopathies encompass various biliary diseases affecting the biliary epithelium, resulting in cholestasis, inflammation, fibrosis, and ultimately liver cirrhosis. Primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC) are the most important progressive cholangiopathies in adults. Much research has broadened the scope of disease biology to genetic risk, epigenetic changes, dysregulated mucosal immunity, altered biliary epithelial cell function, and dysbiosis, all of which interact and arise in the context of ill-defined environmental triggers. An in-depth understanding of the molecular pathogenesis of these cholestatic diseases will help clinicians better prevent and treat diseases. In this review, we focus on the main underlying mechanisms of disease initiation and progression, and novel targeted therapeutics beyond currently approved treatments. Full article

(This article belongs to the Special Issue Cellular and Molecular Pathogenesis of Hepatobiliary Diseases)

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