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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: closed (30 April 2025) | Viewed by 14081

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

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Keywords

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

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Published Papers (5 papers)

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Research

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20 pages, 4516 KiB  
Article
Notch1 siRNA and AMD3100 Ameliorate Metabolic Dysfunction-Associated Steatotic Liver Disease
by Chunli Zhu, Yiheng Cheng, Lei Yang, Yifu Lyu, Jingjing Li, Pengbo Zhao, Ying Zhu, Xiaofei Xin and Lifang Yin
Biomedicines 2025, 13(2), 486; https://doi.org/10.3390/biomedicines13020486 - 16 Feb 2025
Viewed by 892
Abstract
Background and Objectives: As a key mechanism of metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis, inflammation triggered by chronic liver injury and immune cells with macrophages enables MASLD to progress to an advanced stage with irreversible processes such as fibrosis, cell necrosis, [...] Read more.
Background and Objectives: As a key mechanism of metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis, inflammation triggered by chronic liver injury and immune cells with macrophages enables MASLD to progress to an advanced stage with irreversible processes such as fibrosis, cell necrosis, and cancer in the liver. The complexity of MASLD, including crosstalk between multiple organs and the liver, makes developing a new drug for MASLD challenging, especially in single-drug therapy. It was reported that upregulation of Notch1 is closely associated with the function of pro-inflammatory macrophages. To leverage this signaling pathway in treating MASLD, we developed a combination therapy. Materials and Methods: We chose Notch1 siRNA (siNotch1) to block the Notch pathway so that phenotypic regulation and functional recovery can be achieved in macrophages, combining with small molecule drug AMD3100. AMD3100 can cut off the migration of inflammatory cells to the liver to impede the development of inflammation and inhibit the CXCL12/CXCR4 biological axis in liver fibrosis to protect against the activation of HSCs. Then, we investigated the efficacy of the combination therapy on resolving inflammation and MASLD. Results: We demonstrated that in liver cells, siNotch1 combined with AMD3100 not only directly modulated macrophages by downregulating multiple pathways downstream of Notch, exerting anti-inflammatory, anti-migration, and switch of macrophage phenotype, but also modulated macrophage phenotypes through inhibiting NET release. The restored macrophages further regulate HSC and neutrophils. In in vivo pharmacodynamic studies, combination therapy exhibits a superior therapeutical effect over monotherapy in MASLD models. Conclusions: These results constitute an siRNA therapeutical approach combined with a small molecule drug against inflammation and liver injury in MASLD, offering a promising therapeutic intervention for MASLD. Full article
(This article belongs to the Special Issue NASH and Hepatocellular Carcinoma (HCC))
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Review

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18 pages, 1259 KiB  
Review
Locoregional Therapies for Hepatocellular Carcinoma in Patients with Nonalcoholic Fatty Liver Disease
by Stephen Susman, Breanna Santoso and Mina S. Makary
Biomedicines 2024, 12(10), 2226; https://doi.org/10.3390/biomedicines12102226 - 30 Sep 2024
Viewed by 1867
Abstract
Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related death worldwide with an average five-year survival rate in the US of 19.6%. With the advent of HBV and HCV treatment and prevention, along with the rising rates of obesity, nonalcoholic fatty [...] Read more.
Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related death worldwide with an average five-year survival rate in the US of 19.6%. With the advent of HBV and HCV treatment and prevention, along with the rising rates of obesity, nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome are set to overtake infectious causes as the most common cause of HCC. While surgical resection and transplantation can be curative when amenable, the disease is most commonly unresectable on presentation, and other treatment approaches are the mainstay of therapy. In these patients, locoregional therapies have evolved as a vital tool in both palliation for advanced disease and as a bridge to surgical resection and transplantation. In this review, we will be exploring the primary locoregional therapies for HCC in patients with NAFLD, including transarterial chemoembolization (TACE), bland transarterial embolization (TAE), transarterial radioembolization (TARE), and percutaneous ablation. Full article
(This article belongs to the Special Issue NASH and Hepatocellular Carcinoma (HCC))
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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
Cited by 7 | Viewed by 3683
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 13 | Viewed by 2340
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 35 | Viewed by 4393
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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