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Life
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Liver Disease: Pathogenesis, Diagnosis, and Treatments
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Liver Disease: Pathogenesis, Diagnosis, and Treatments

A Special Issue of Life (ISSN 2075-1729) belonging to the section "Medical Research".

Deadline for manuscript submissions: 25 September 2026 | Viewed by 9571

Editor

Dr. Hsien-Hui Chung

E-Mail Website
Guest Editor
Preventive Medicine Program, Center for General Education, Chung Yuan Christian University, Taoyuan City 320314, Taiwan
Interests: diabetes; endocrinology; gastroenterology; hepatology; pharmacology

Special Issue Information

Dear Colleagues,

Liver diseases have led to a higher prevalence of deaths worldwide, including viral hepatitis, metabolic dysfunction-associated steatohepatitis (MASH), alcoholic hepatitis, and liver cancer. Although many prescription drugs have been used for the treatment of the aforementioned liver diseases, therapy resistance and complicated pathogenesis still contribute to therapeutic failure and challenges. In this Special Issue, we are interested in publishing the latest research relating to hepatology, as well as advances in the areas related to pathogenesis, diagnosis, novel targets and biomarkers, molecular mechanisms, therapeutic strategies, and new drug development. Thus, more precise medicine against liver diseases can give patients a better quality of life.

In this Special Issue, original research articles and review articles are welcome. Research areas may include, but are not limited, to the following items:

  • Drug development against liver diseases;
  • Experimental hepatology;
  • Liver disease targets and biomarkers;
  • Metabolic syndrome-induced liver diseases;
  • Molecular mechanisms of liver diseases;
  • Precise therapeutics for liver diseases.

Dr. Hsien-Hui Chung
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life 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

  • alcoholic hepatitis
  • artificial intelligence
  • biomarkers
  • clinical trials
  • gut–liver axis
  • liver cancer
  • metabolic dysfunction-associated steatohepatitis
  • molecular targets
  • pharmacotherapeutic mechanisms
  • therapeutic strategies

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (5 papers)

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Research

Jump to: Review, Other

12 pages, 1009 KB  
Article
Clinical Prognostic Factors and Survival Risk Stratification for Advanced Biliary Tract Cancer Treated with Gemcitabine-Based Palliative Chemotherapy: A Real-World Retrospective Study
by Jirapat Wonglhow, Arunee Dechaphunkul, Patrapim Sunpaweravong, Chirawadee Sathitruangsak and Panu Wetwittayakhlang
Life 2026, 16(7), 1176; https://doi.org/10.3390/life16071176 - 16 Jul 2026
Viewed by 353
Abstract
Background: Although gemcitabine-based palliative chemotherapy remains widely used for advanced biliary tract cancer (BTC), practical pretreatment prognostic factors are needed. This study identified baseline prognostic factors associated with overall survival (OS) and explored a simple risk stratification approach for 12-month survival in advanced [...] Read more.
Background: Although gemcitabine-based palliative chemotherapy remains widely used for advanced biliary tract cancer (BTC), practical pretreatment prognostic factors are needed. This study identified baseline prognostic factors associated with overall survival (OS) and explored a simple risk stratification approach for 12-month survival in advanced BTC patients treated with gemcitabine-based chemotherapy. Methods: This retrospective cohort study included advanced BTC patients treated with gemcitabine-based palliative chemotherapy between 2011 and 2025. Baseline clinical and laboratory variables were collected at treatment initiation. The Kaplan–Meier method estimated OS. Univariable and multivariable Cox proportional hazards regression analyses identified prognostic factors. A post hoc exploratory risk score was developed using routinely available factors independently associated with OS. Results: A total of 154 patients were included, gemcitabine plus cisplatin was administered to 95 patients, whereas 59 received gemcitabine plus carboplatin. Median OS was 9.43 months. Multivariable analysis showed that ECOG performance status ≥ 2 (adjusted HR, 5.68; 95% CI, 2.52–12.81), alkaline phosphatase (ALP) ≥ 2 × ULN (adjusted HR, 1.53; 95% CI, 1.01–2.33), and neutrophil-to-lymphocyte ratio (NLR) ≥ 3 (adjusted HR, 1.51; 95% CI, 1.03–2.20) were associated with worse OS. An exploratory score assigning one point to each factor stratified patients into low-, intermediate-, and high-risk groups. The estimated 12-month OS rates were 59.6%, 40.4%, and 10.8%, respectively. Conclusions: Poor performance status, elevated ALP, and elevated NLR were associated with worse OS in advanced BTC patients receiving gemcitabine-based palliative chemotherapy. However, the associations for ALP and NLR were modest and should be interpreted cautiously. A simple exploratory score based on routinely available factors demonstrated distinct 12-month survival across risk groups and may help inform prognostic discussions in routine practice. This approach should be considered hypothesis-generating, and external validation is warranted. Full article
(This article belongs to the Special Issue Liver Disease: Pathogenesis, Diagnosis, and Treatments)
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17 pages, 6413 KB  
Article
Modulation of Oxidative and ER Stress Pathways by the ADAM17 Inhibitor GW280264X in LPS-Induced Acute Liver Injury
by Merve Huner Yigit, Oguzhan Okcu, Mehtap Atak, Soner Karabulut, Gökhan Yıldız and Ertugrul Yigit
Life 2025, 15(12), 1877; https://doi.org/10.3390/life15121877 - 8 Dec 2025
Cited by 2 | Viewed by 1132
Abstract
Background and Objectives: ADAM17, a sheddase that regulates cytokine and receptor ectodomains, amplifies inflammatory signaling. Acute liver injury (ALI) is driven by dysregulated inflammation, accompanied by both oxidative and endoplasmic reticulum (ER) stress responses. We investigated whether pharmacological inhibition of ADAM17 with GW280264X [...] Read more.
Background and Objectives: ADAM17, a sheddase that regulates cytokine and receptor ectodomains, amplifies inflammatory signaling. Acute liver injury (ALI) is driven by dysregulated inflammation, accompanied by both oxidative and endoplasmic reticulum (ER) stress responses. We investigated whether pharmacological inhibition of ADAM17 with GW280264X mitigates lipopolysaccharide (LPS)-induced acute liver injury by targeting these pathways. Methods: Male C57BL/6J mice received intraperitoneal LPS (10 mg/kg). GW280264X (500 µg/kg, i.p.) was administered at one and three hours post-LPS treatment. At the fifth hour, serum and liver samples were collected to determine serum ALT/AST levels and to perform hematoxylin and eosin (H&E) staining. Inflammatory (TNF-α), oxidative (MDA, 4-HNE, Fe2+, GSH; NRF2/KEAP1), endoplasmic reticulum (ER) stress (GRP78, ATF6, CHOP), and ferroptosis-related (GPX4, SLC7A11) markers, along with ADAM17 protein levels, were analyzed using ELISA, colorimetric assays, and Western blotting. Results: LPS triggered hepatic injury. This was accompanied by marked elevations in TNF-α, oxidative indices (MDA, 4-HNE, Fe2+) and ER stress proteins (GRP78, ATF6, CHOP), together with depletion of hepatic GSH. GW280264X significantly reduced AST levels, attenuated inflammatory, oxidative, and ER stress responses, and improved hepatic histopathology. GPX4 and SLC7A11 tended to increase following treatment, but the changes did not reach statistical significance and should be interpreted cautiously due to the limited sample size (n = 5). Similarly, ADAM17 protein levels tended to decrease, although the change was not statistically significant. Conclusions: Pharmacological inhibition of ADAM17 with GW280264X may confer early hepatoprotection in LPS-induced ALI by attenuating inflammatory, oxidative and ER stress pathways. ADAM17 inhibition yielded partial and statistically non-significant protective effects at this early stage; therefore, these findings should be considered exploratory. Future studies with larger sample sizes and longer observation periods are warranted to confirm the durability and mechanistic basis of this response. Full article
(This article belongs to the Special Issue Liver Disease: Pathogenesis, Diagnosis, and Treatments)
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Review

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12 pages, 1423 KB  
Review
Metabolic Concepts of Sodium-Glucose Cotransporter 2 Inhibitors-Based Therapies Against Hepatocarcinogenesis and Therapy Resistance in Hepatocellular Carcinoma
by Hsien-Hui Chung
Life 2026, 16(3), 446; https://doi.org/10.3390/life16030446 - 10 Mar 2026
Viewed by 846
Abstract
The prevalence of hepatocellular carcinoma (HCC) has increased in recent years and resulted in many deaths, which necessitates new therapeutic solutions. The pathogenesis of HCC is associated with uncontrolled metabolic modulation and resistance to therapy. As diabetic carcinogenesis accelerates HCC progression, proper evaluation [...] Read more.
The prevalence of hepatocellular carcinoma (HCC) has increased in recent years and resulted in many deaths, which necessitates new therapeutic solutions. The pathogenesis of HCC is associated with uncontrolled metabolic modulation and resistance to therapy. As diabetic carcinogenesis accelerates HCC progression, proper evaluation of anti-diabetic drugs to attenuate HCC is important. Although sodium-glucose cotransporter 2 (SGLT2) inhibitors that suppress renal SGLT2 are beneficial for treating diabetes, chronic kidney diseases, and heart failure, the use of SGLT2 inhibitors for treating HCC remains unclear. In this review article, some oncotargets involved in metabolic reprogramming, including glucose metabolism, Wnt/β-catenin, and hypoxia-inducible factor-1 alpha signaling, and the tumor microenvironment of HCC are briefly highlighted. Moreover, upregulated SGLT2 expression may be associated with hepatocarcinogenesis and therapy resistance, whereas the incorporation of SGLT2 inhibitors into combination therapies effectively attenuates HCC progression, metastasis, and therapy resistance through multiple mechanisms. Notably, how SGLT2 inhibitors modulate immune responses to cancer vaccines against HCC is highly appreciated and requires further evaluation. Thus, the clinical application of SGLT2 inhibitors in HCC and therapy resistance provides a promising direction for therapeutic strategies. Full article
(This article belongs to the Special Issue Liver Disease: Pathogenesis, Diagnosis, and Treatments)
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18 pages, 458 KB  
Review
Improvement of Liver Fibrosis in Patients with MASLD Undergoing Pioglitazone Treatment: An Update
by Cristina Stasi and Andrea Mega
Life 2025, 15(11), 1682; https://doi.org/10.3390/life15111682 - 29 Oct 2025
Cited by 4 | Viewed by 4759
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is defined as steatotic liver disease with at least one cardiometabolic risk factor, in the absence of harmful alcohol intake, and includes a spectrum of conditions. These range from isolated liver steatosis to metabolic dysfunction-associated steatohepatitis (MASH), [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is defined as steatotic liver disease with at least one cardiometabolic risk factor, in the absence of harmful alcohol intake, and includes a spectrum of conditions. These range from isolated liver steatosis to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis, and MASH-related hepatocellular carcinoma. Patients with MASLD and type 2 diabetes are at increased risk of developing MASH and significant/advanced fibrosis. The severity of fibrosis is a key determinant of long-term prognosis in MASLD. The most recent AASLD and EASL-EASD-EASO Guidelines on the Management of MASLD recommend a step-by-step approach to identify patients at higher risk of fibrotic progression. Recent epidemiological trends highlight the socioeconomic impact of MASLD and MASH, particularly in middle- and low-income countries. Given the high cost of new targeted therapies, implementing effective treatment strategies in low-resource settings is essential in managing MASLD and MASH patients. Pioglitazone is an oral antidiabetic agent of the thiazolidinedione class that targets peroxisome proliferator-activated receptors activated by fatty acids and derivatives or pharmacological agonists and involved in lipid metabolism, cell differentiation, and inflammation. Pioglitazone treatment is a potential cost-effective option, particularly for low-resource settings. This review examines recent epidemiological trends in MASLD and MASH, outlines the mechanisms of action of pioglitazone with an emphasis on its role in improving liver fibrosis, and summarizes clinical studies on fibrosis evaluation during pioglitazone treatment. The literature search focused on English-language studies from the past two years in the PubMed database. Full article
(This article belongs to the Special Issue Liver Disease: Pathogenesis, Diagnosis, and Treatments)
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Other

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13 pages, 1916 KB  
Case Report
Herb-Induced Liver Injury by Laurus nobilis: A Case Assessed for Causality Using the Updated RUCAM
by Mihnea Soare, Sabina-Florina Călugăr-Șolea, Ciprian Brisc, Marius Rus, Teodora-Maria Bodog, Gabriel Becheanu, Ciprian Mihai Brisc and Mihaela-Cristina Brisc
Life 2026, 16(1), 180; https://doi.org/10.3390/life16010180 - 22 Jan 2026
Viewed by 1429
Abstract
Hepatocellular injury syndrome represents a pathological process with a broad etiological spectrum, including viral infections, autoimmune diseases, or intoxications. Clinicians must identify the potential cause using both anamnestic data and available paraclinical examinations. We present the case of a 55-year-old female patient, admitted [...] Read more.
Hepatocellular injury syndrome represents a pathological process with a broad etiological spectrum, including viral infections, autoimmune diseases, or intoxications. Clinicians must identify the potential cause using both anamnestic data and available paraclinical examinations. We present the case of a 55-year-old female patient, admitted to the Internal Medicine 1 Department at the Clinical County Emergency Hospital Bihor, Oradea, Romania. The patient exhibited nonspecific complaints and insignificant pathological antecedents, but from a biochemical perspective, substantial changes in liver transaminase levels were evident. To establish differential diagnoses, a series of biochemical and immunological tests were performed, along with a thorough medical history. It was concluded that the patient regularly consumes herbal infusions, specifically Laurus nobilis leaves, commonly known as Bay Laurel. Although this might be easily overlooked at first glance, a closer examination could explain the current clinical picture. In April 2024, a 55-year-old female patient with no history of liver pathology was admitted. She complained of asthenia fatigue, anorexia, mixed dyspeptic symptoms, diffuse abdominal pain, and a weight loss of 12 kg. The pathology had insidiously started approximately 3 months prior. On examination, the patient had altered general status, anorexia, and was overweight. Biochemically, the patient had elevated liver transaminase values (AST = 196 U/L and ALT = 357 U/L) that continued to rise during hospitalization, despite hepatoprotective treatment. Various paraclinical examinations were performed to exclude other potential causes of hepatic aggression, having excluded ordinary causes. Consequently, a liver biopsy was performed, and the histopathological examination leaned toward a toxic hepatitis etiology. Application of the updated RUCAM scale yielded a score of eight points (“probable” HILI—Herb-Induced Liver Injury). Clinical and biochemical improvement was observed after complete cessation of bay leaf tea consumption. This case highlights the potential hepatotoxicity of commonly used culinary herbs when consumed in large quantities or as concentrated infusions and emphasizes the importance of detailed anamnesis regarding herbal product use. Full article
(This article belongs to the Special Issue Liver Disease: Pathogenesis, Diagnosis, and Treatments)
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