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Cirrhosis: From Molecular Mechanisms to Therapeutic Strategies
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Cirrhosis: From Molecular Mechanisms to Therapeutic Strategies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 December 2025 | Viewed by 2019

Special Issue Editor

Dr. Hongqun Liu

E-Mail Website
Guest Editor
Liver Unit, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada
Interests: hepatology

Special Issue Information

Dear Colleagues,

Cirrhosis is the end‐stage of chronic liver disease. The process of cirrhosis development includes inflammation, hepatocyte necrosis, extracellular matrix deposition, fibrotic tissue proliferation and regenerative nodule formation. Long‐term inflammation, necrosis and fibrotic tissue proliferation cause continuous damage of the liver, the formation of scar tissue and lobular nodules, and eventually result in cirrhosis and portal hypertension. During this process, fibrogenesis is essential; therefore, antifibrosis strategies are the key to treating patients with cirrhosis or postponing the process of fibrogenesis. Although there are many studies on therapeutic strategies aimed at reversing or preventing fibrosis, their efficacy is not optimistic. Studies aimed at investigating molecular mechanisms and improving therapeutic efficacy remain necessary.

Another important aspect is the treatment of complications of patients with cirrhosis, such as hepatorenal syndrome, cirrhotic cardiomyopathy, acute on chronic liver failure, and hepatic encephalopathy. Studies on the molecular mechanisms and therapeutic strategies of these complications improve the managements of these patients.

The aim of this Special Issue, “Cirrhosis: From Molecular Mechanisms to Therapeutic Strategies”, is to summarize/update the status of the studies in this field. This Special Issue will collate updated articles, including original research, narrative reviews, systematic reviews, and meta-analyses.

Dr. Hongqun Liu
Guest Editor

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • liver
  • fibrogenesis
  • cirrhosis
  • portal hypertension
  • complications
  • molecular mechanisms
  • pathway
  • therapeutic strategies

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Published Papers (4 papers)

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Research

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15 pages, 2410 KiB  
Article
Differences in Tissue Copper and Zinc Content Between Normal Livers and Those with Cirrhosis with or Without Hepatocellular Carcinoma
by Simona Parisse, Giulia Andreani, Monica Mischitelli, Alessandra Gianoncelli, Emil Malucelli, Michela Fratini, Flaminia Ferri, Maria Carlucci, Quirino Lai, Andrea Ascione, Gianluca Mennini, Massimo Rossi, Stefano Iotti, Gloria Isani and Stefano Ginanni Corradini
Int. J. Mol. Sci. 2025, 26(14), 6571; https://doi.org/10.3390/ijms26146571 - 8 Jul 2025
Viewed by 296
Abstract
This study aimed to compare the contents of copper (Cu), zinc (Zn), magnesium (Mg), and iron (Fe) in healthy liver tissue from deceased liver donors (DGs), in cirrhotic tissue from patients without (CIR) or with hepatocellular carcinoma (CIR-HCC) and in HCC tissue from [...] Read more.
This study aimed to compare the contents of copper (Cu), zinc (Zn), magnesium (Mg), and iron (Fe) in healthy liver tissue from deceased liver donors (DGs), in cirrhotic tissue from patients without (CIR) or with hepatocellular carcinoma (CIR-HCC) and in HCC tissue from the latter patients. Liver tissue samples were obtained from cirrhotic liver transplant recipients, with (n = 14) and without HCC (n = 14), and from DGs (n = 18). In patients with HCC, both cirrhotic and tumor tissue was collected. The tissue metal content was measured using atomic absorption spectrometry. The Cu content of DG tissue was significantly lower than that of CIR-HCC and HCC tissue but not CIR tissue. The tissue Zn and Mg contents were significantly higher in DG tissue than in CIR, CIR-HCC, and HCC tissues. No difference was observed for Fe. The Cu/Zn ratio progressively increased in DG, CIR, CIR-HCC, and HCC tissues. The increased Cu content in cirrhotic and tumor tissue of HCC patients and the fact that the latter had the highest value for the Cu/Zn ratio indirectly suggest the potential role of these metals in hepatocarcinogenesis. These findings support a pathophysiological basis for further experimental studies to investigate the potential therapeutic implications of pharmacological agents targeting metal homeostasis in this malignancy. Full article
(This article belongs to the Special Issue Cirrhosis: From Molecular Mechanisms to Therapeutic Strategies)
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Review

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26 pages, 2576 KiB  
Review
Exploring Cirrhosis: Insights into Advances in Therapeutic Strategies
by Magdalena Wiacek, Anna Adam, Rafał Studnicki and Igor Z. Zubrzycki
Int. J. Mol. Sci. 2025, 26(15), 7226; https://doi.org/10.3390/ijms26157226 - 25 Jul 2025
Viewed by 204
Abstract
Cirrhosis remains a significant global health burden, responsible for nearly 4% of annual deaths worldwide. Despite progress in antiviral therapies and public health measures, its prevalence has plateaued, particularly in regions affected by viral hepatitis, alcohol misuse, and metabolic syndrome. This review presents [...] Read more.
Cirrhosis remains a significant global health burden, responsible for nearly 4% of annual deaths worldwide. Despite progress in antiviral therapies and public health measures, its prevalence has plateaued, particularly in regions affected by viral hepatitis, alcohol misuse, and metabolic syndrome. This review presents a comprehensive synthesis of the multifactorial drivers of cirrhosis, including hepatocyte injury, liver stellate cell activation, and immune-mediated inflammation. The emphasis is on the central role of metabolic dysfunction, characterized by mitochondrial impairment, altered lipid and glucose metabolism, hormonal imbalance, and systemic inflammation, in exacerbating disease progression. While current therapies may slow the progression of early-stage disease, they are very often ineffective in reversing established fibrosis. Emerging molecular strategies offer promising alternatives by targeting key pathogenic pathways. These include AMPK activators (e.g., metformin, AICAR), FGF21 analogs, and mitochondria-targeted agents (e.g., MitoQ, urolithin A, NAD+ precursors) to restore bioenergetic balance and reduce oxidative stress. Other approaches, such as mesenchymal stem cell therapy, inflammasome inhibition, and hormonal modulation, aim to suppress fibrogenesis and restore liver homeostasis. The integration of systems biology and multi-omics profiling supports patient stratification and precision medicine. This review highlights a shift toward mechanism-based interventions that have the potential to alter cirrhosis outcomes and improve patient survival. Full article
(This article belongs to the Special Issue Cirrhosis: From Molecular Mechanisms to Therapeutic Strategies)
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Graphical abstract

14 pages, 1449 KiB  
Review
Apoptosis in Cardiac Conditions Including Cirrhotic Cardiomyopathy
by Fengxue Yu, Dae Gon Ryu, Ki Tae Yoon, Hongqun Liu and Samuel S. Lee
Int. J. Mol. Sci. 2025, 26(13), 6423; https://doi.org/10.3390/ijms26136423 - 3 Jul 2025
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Abstract
Apoptosis is a highly regulated process of programmed cell death and plays a crucial pathogenic role in a variety of conditions including cardiovascular diseases. There are two pathways leading to apoptosis, the intrinsic and extrinsic pathways. In the intrinsic pathway, also known as [...] Read more.
Apoptosis is a highly regulated process of programmed cell death and plays a crucial pathogenic role in a variety of conditions including cardiovascular diseases. There are two pathways leading to apoptosis, the intrinsic and extrinsic pathways. In the intrinsic pathway, also known as the mitochondria-mediated pathway, the cell kills itself because it senses cell stress. Mitochondria account for 30% of cardiomyocyte volume, and therefore, the heart is vulnerable to apoptosis. The extrinsic pathway, also known as the death receptor-mediated pathway, is initiated by death receptors, members of the tumor necrosis factor receptor gene superfamily. Excessive apoptosis is involved in cardiac dysfunction in different cardiac conditions, including heart failure, ischemic heart disease, and cirrhotic cardiomyopathy. The last entity is a serious cardiac complication of patients with cirrhosis. To date, there is no effective treatment for cirrhotic cardiomyopathy. The conventional treatments for non-cirrhotic heart failure such as vasodilators are not applicable due to the generalized peripheral vasodilatation in cirrhotic patients. Exploring new approaches for the treatment of cirrhotic cardiomyopathy is therefore of utmost importance. Since apoptosis plays an essential role in the pathogenesis and progression of cardiovascular conditions, anti-apoptotic treatment could potentially prevent/attenuate the development and progression of cardiac diseases. Anti-apoptotic treatment may also apply to cirrhotic cardiomyopathy. The present review summarizes apoptotic mechanisms in different cardiac diseases, including cirrhotic cardiomyopathy, and potential therapies to regulate apoptosis in these conditions. Full article
(This article belongs to the Special Issue Cirrhosis: From Molecular Mechanisms to Therapeutic Strategies)
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Other

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12 pages, 818 KiB  
Brief Report
Clinical Significance of Marginal Zinc Deficiency as a Predictor of Covert Hepatic Encephalopathy in Patients with Liver Cirrhosis
by Takuya Matsuda, Tadashi Namisaki, Akihiko Shibamoto, Shohei Asada, Fumimasa Tomooka, Takahiro Kubo, Aritoshi Koizumi, Misako Tanaka, Satoshi Iwai, Takashi Inoue, Yuki Tsuji, Yukihisa Fujinaga, Norihisa Nishimura, Shinya Sato, Koh Kitagawa, Kosuke Kaji, Akira Mitoro, Kiyoshi Asada, Hiroaki Takaya, Ryuichi Noguchi, Takemi Akahane and Hitoshi Yoshijiadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2025, 26(9), 4184; https://doi.org/10.3390/ijms26094184 - 28 Apr 2025
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Abstract
Covert hepatic encephalopathy (CHE) can worsen the quality of life and prognosis of patients with cirrhosis. We analyzed the risk factors of CHE and identified patients at high risk for overt hepatic encephalopathy (HE) who would benefit from therapeutic interventions. We included 145 [...] Read more.
Covert hepatic encephalopathy (CHE) can worsen the quality of life and prognosis of patients with cirrhosis. We analyzed the risk factors of CHE and identified patients at high risk for overt hepatic encephalopathy (HE) who would benefit from therapeutic interventions. We included 145 patients without a history of or treatment for overt HE. Patients were divided into the CHE and no-CHE groups (n = 91 and 54, respectively). CHE had a score above the age-based cutoff value of one of the neuropsychological tests, such as the Stroop and number connection tests. CHE prevalence was 62.8% (n = 91). Compared with the no-CHE group, the CHE group had significantly lower serum zinc and albumin levels. Multiple logistic regression analysis identified serum zinc levels at a cutoff value of 74 µg/dL. Subclinical zinc deficiency showed a diagnostic performance of 55.6% sensitivity and 81.5% specificity for CHE. Blood ammonia levels and liver functional reserves were not predictive of CHE. Compared with patients with zinc levels < 74 µg/dL (n = 102), those with ≥74 µg/dL (n = 43) had significantly lower CHE prevalence and better hepatic functional reserve. Subclinical zinc deficiency was associated with CHE occurrence in patients with cirrhosis without a history of or treatment for overt HE. Measurement of zinc levels facilitates early detection of CHE by neuropsychological testing. Full article
(This article belongs to the Special Issue Cirrhosis: From Molecular Mechanisms to Therapeutic Strategies)
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