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Biomedicines
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NASH and Hepatocellular Carcinoma (HCC)
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NASH and Hepatocellular Carcinoma (HCC)

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 4293

Special Issue Editor

Dr. Feng He

E-Mail Website
Guest Editor
The Center for Cancer Research, Academy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China
Interests: obesity; NASH; Hepatocellular Carcinoma (HCC)

Special Issue Information

Dear Colleagues,

Caloric excess and sedentary lifestyle are growing health concerns that have led to a global epidemic of obesity and metabolic syndrome. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of obesity and metabolic syndrome, is a major cause of liver disease worldwide and its prevalence is increasing in parallel with obesity and type 2 diabetes. This spectrum of NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis, which ultimately leads to hepatocellular carcinoma (HCC), a leading cause of cancer-related deaths worldwide. Liver damage associated with NASH leads to a cycle of cell death, liver regeneration, and fibrosis, during which HCC precursor cells undergo malignant transformation, leading to cancer initiation. Several mechanisms have been proposed to underlie the progression of NASH to cirrhosis, and eventually HCC, including cell death, ER stress, mitochondrial dysfunction, inflammation, and oxidative stress. The mechanisms of progression of NASH, fibrosis, and HCC are far from being understood.

In this Special Issue, we aim to present a series of review and research articles that elucidate the progression in the diagnosis, prevention, and treatment of NASH and HCC, along with the many challenges that still remain. We welcome basic, translational, or clinical studies that contribute to our new understanding of disease progression from NASH and HCC as well as potential new therapies.

Dr. Feng He
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

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

  • NAFLD
  • NASH
  • HCC
  • obesity
  • inflammation
  • immunotherapy
  • stress

Published Papers (3 papers)

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Review

12 pages, 883 KiB  
Review
Namodenoson at the Crossroad of Metabolic Dysfunction-Associated Steatohepatitis and Hepatocellular Carcinoma
by Ohad Etzion, Avital Bareket-Samish, David Yardeni and Pnina Fishman
Biomedicines 2024, 12(4), 848; https://doi.org/10.3390/biomedicines12040848 - 11 Apr 2024
Viewed by 882
Abstract
Namodenoson (CF102) is a small, orally available, anti-inflammatory, and anti-cancer drug candidate currently in phase 2B trial for the treatment of metabolic dysfunction-associated steatohepatitis (MASH; formerly known as non-alcoholic steatohepatitis (NASH)) and in phase 3 pivotal clinical trial for the treatment of hepatocellular [...] Read more.
Namodenoson (CF102) is a small, orally available, anti-inflammatory, and anti-cancer drug candidate currently in phase 2B trial for the treatment of metabolic dysfunction-associated steatohepatitis (MASH; formerly known as non-alcoholic steatohepatitis (NASH)) and in phase 3 pivotal clinical trial for the treatment of hepatocellular carcinoma (HCC). In both MASH and HCC, the mechanism-of-action of namodenoson involves targeting the A3 adenosine receptor (A3AR), resulting in deregulation of downstream signaling pathways and leading to inhibition of inflammatory cytokines (TNF-α, IL-1, IL-6, and IL-8) and stimulation of positive cytokines (G-CSF and adiponectin). Subsequently, inhibition of liver inflammation, steatosis, and fibrosis were documented in MASH experimental models, and inhibition of HCC growth was observed in vitro, in vivo, and in clinical studies. This review discusses the evidence related to the multifaceted mechanism of action of namodenoson, and how this mechanism is reflected in the available clinical data in MASH and HCC. Full article
(This article belongs to the Special Issue NASH and Hepatocellular Carcinoma (HCC))
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14 pages, 299 KiB  
Review
The Outcomes of Liver Transplantation in Severe Metabolic Dysfunction-Associated Steatotic Liver Disease Patients
by Natasa Paklar, Maja Mijic and Tajana Filipec-Kanizaj
Biomedicines 2023, 11(11), 3096; https://doi.org/10.3390/biomedicines11113096 - 20 Nov 2023
Cited by 1 | Viewed by 1095
Abstract
The increasing prevalence of diabetes mellitus, obesity, and metabolic syndrome in the population can lead to metabolic dysfunction-associated steatohepatitis (MASH) and metabolic dysfunction-associated steatotic liver disease (MASLD). In Western industrialized countries, this has become a major problem with significant socioeconomic impacts. MASH is [...] Read more.
The increasing prevalence of diabetes mellitus, obesity, and metabolic syndrome in the population can lead to metabolic dysfunction-associated steatohepatitis (MASH) and metabolic dysfunction-associated steatotic liver disease (MASLD). In Western industrialized countries, this has become a major problem with significant socioeconomic impacts. MASH is now a leading cause of liver transplantation (LT), especially in developed countries. However, the post-transplant outcomes of such patients are a major concern, and published data are limited and extremely variable. In this article, we discuss graft and patient survival after LT, complications, the recurrence of MASH, and MASH appearing de novo after transplantation. Recent studies suggest that patients with MASH have slightly worse short-term survival, potentially due to increased cardiovascular mortality. However, most studies found that longer-term outcomes for patients undergoing LT for MASH are similar or even better than those for other indications. Hepatocellular carcinoma due to MASH cirrhosis also has similar or even better outcomes after LT than other etiologies. In conclusion, we suggest questions and topics that require further research to enhance healthcare for this growing patient population. Full article
(This article belongs to the Special Issue NASH and Hepatocellular Carcinoma (HCC))
15 pages, 7336 KiB  
Review
Pathology and Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease-Associated Hepatic Tumors
by Yoshihisa Takahashi, Erdenetsogt Dungubat, Hiroyuki Kusano and Toshio Fukusato
Biomedicines 2023, 11(10), 2761; https://doi.org/10.3390/biomedicines11102761 - 12 Oct 2023
Cited by 6 | Viewed by 1870
Abstract
Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive fat accumulation in the livers of patients without a history of alcohol abuse. It is classified as either simple steatosis (nonalcoholic fatty liver) or nonalcoholic steatohepatitis (NASH), which can progress to liver cirrhosis and [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive fat accumulation in the livers of patients without a history of alcohol abuse. It is classified as either simple steatosis (nonalcoholic fatty liver) or nonalcoholic steatohepatitis (NASH), which can progress to liver cirrhosis and hepatocellular carcinoma (HCC). Recently, it was suggested that the terms “metabolic dysfunction-associated steatotic liver disease (MASLD)” and “metabolic dysfunction-associated steatohepatitis (MASH)” should replace the terms “nonalcoholic fatty liver disease (NAFLD)” and “nonalcoholic steatohepatitis (NASH)”, respectively, with small changes in the definitions. MASLD, a hepatic manifestation of metabolic syndrome, is rapidly increasing in incidence globally, and is becoming an increasingly important cause of HCC. Steatohepatitic HCC, a histological variant of HCC, is characterized by its morphological features resembling non-neoplastic steatohepatitis and is closely associated with underlying steatohepatitis and metabolic syndrome. Variations in genes including patatin-like phospholipase domain-containing protein 3 (PNPLA3), transmembrane 6 superfamily 2 (TM6SF2), and membrane-bound O-acyltransferase domain-containing protein 7 (MBOAT7) are associated with the natural history of MASLD, including HCC development. The mechanisms of HCC development in MASLD have not been fully elucidated; however, various factors, including lipotoxicity, inflammation, reactive oxygen species, insulin resistance, and alterations in the gut bacterial flora, are important in the pathogenesis of MASLD-associated HCC. Obesity and MASLD are also recognized as risk factors for hepatocellular adenomas, and recent meta-analyses have shown an association between MASLD and intrahepatic cholangiocarcinoma. In this review, we outline the pathology and pathogenesis of MASLD-associated liver tumors. Full article
(This article belongs to the Special Issue NASH and Hepatocellular Carcinoma (HCC))
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