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Biomolecules
Special Issues
Liver Damage and Associated Metabolic Disorders
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Liver Damage and Associated Metabolic Disorders

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 7015

Special Issue Editor

Dr. Lin Jia

E-Mail Website
Guest Editor
Department of Biological Sciences, The University of Texas at Dallas, Richardson, TX, USA
Interests: hepatic steatosis; advanced liver injury; insulin resistance; inflammation; dyslipidemia; thermogenesis; alcohol; organ crosstalk

Special Issue Information

Dear Colleagues,

The liver is an essential organ of the body that performs over 500 vital functions. These include removing waste products and foreign substances from the bloodstream, regulating blood sugar levels, and creating essential nutrients. The liver is implicated in many processes, and its failure induces severe consequences for metabolism, immune response, detoxification, and antimicrobial defenses. Metabolic dysfunction-associated fatty liver disease (MAFLD) is one of the most common chronic liver diseases worldwide. The close relationship with epidemic obesity and metabolic abnormalities and the potential progression towards end-stage liver diseases, such as cirrhosis and HCC, make MAFLD an emerging global health problem.

This Special Issue aims to gather original findings and intriguing hypotheses related to liver damage caused by a range of stimuli and associated metabolic disorders, including dyslipidemia, insulin resistance, and chronic inflammation. Research areas may include (but are not limited to) the following: molecular and cellular mechanisms in the pathogenesis of liver damage; genetic and epigenetic factors in liver disease risk; lipid dysregulation in disease initiation and progression; interactions between the liver and other organs in the development of metabolic syndrome; biomarkers; and therapeutic strategies for acute and chronic liver disease.

Both original research articles and reviews are welcome. We look forward to receiving your contributions.

Dr. Lin Jia
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. Biomolecules 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 2700 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

  • lipid species
  • lipid metabolism
  • organelle dynamics
  • hepatokines
  • metabolic risk
  • immune responses

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Published Papers (4 papers)

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Research

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15 pages, 1880 KiB  
Article
High-Sensitivity C-Reactive Protein Levels in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), Metabolic Alcohol-Associated Liver Disease (MetALD), and Alcoholic Liver Disease (ALD) with Metabolic Dysfunction
by Seong-Uk Baek and Jin-Ha Yoon
Biomolecules 2024, 14(11), 1468; https://doi.org/10.3390/biom14111468 - 18 Nov 2024
Cited by 2 | Viewed by 1653
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a recently introduced term for steatotic liver disease (SLD). Although the inflammatory process is central to the pathogenesis of SLD, research investigating the differences in systemic inflammation across various SLD subtypes as well as sex differences [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a recently introduced term for steatotic liver disease (SLD). Although the inflammatory process is central to the pathogenesis of SLD, research investigating the differences in systemic inflammation across various SLD subtypes as well as sex differences is limited. This population-based, cross-sectional study investigated the association between SLD subtypes and high-sensitivity C-reactive protein (hs-CRP) levels among Korean adults (N = 20,141; mean age: 50.8 ± 16.7 years). The participants were classified into five groups that included no SLD, MASLD, metabolic alcohol-associated liver disease (MetALD), alcoholic liver disease with metabolic dysfunction (ALD with MD), and other SLDs. The median (Q1, Q3) value of the hs-CRP level was 0.54 mg/L (0.33, 1.04). Among men, compared to levels in the no SLD group, the MASLD, MetALD, and ALD with MD groups were associated with 41.9% (95% confidence interval [CI]: 35.1–49.1%), 46.8% (95% CI: 35.0–59.6%), and 51.8% (95% CI: 30.0–77.2%) increases in hs-CRP levels, respectively. The association between SLD subtypes and hs-CRP levels was stronger among women, and compared to the levels in the no SLD group, the MASLD, MetALD, and ALD with MD groups were associated with 81.5% (95% CI: 73.6–89.8%), 84.3% (95% CI: 58.1–114.8%), and 98.2% (95% CI: 38.0–184.8%) increases in hs-CRP levels, respectively. In conclusion, our findings indicate a varying profile of systemic inflammation across SLD subtypes, with more pronounced increases in hs-CRP levels in women with SLDs. Full article
(This article belongs to the Special Issue Liver Damage and Associated Metabolic Disorders)
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18 pages, 2681 KiB  
Article
The Development of a Non-Invasive Screening Method Based on Serum microRNAs to Quantify the Percentage of Liver Steatosis
by Polina Soluyanova, Guillermo Quintás, Álvaro Pérez-Rubio, Iván Rienda, Erika Moro, Marcel van Herwijnen, Marcha Verheijen, Florian Caiment, Judith Pérez-Rojas, Ramón Trullenque-Juan, Eugenia Pareja and Ramiro Jover
Biomolecules 2024, 14(11), 1423; https://doi.org/10.3390/biom14111423 - 8 Nov 2024
Cited by 1 | Viewed by 1632
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is often asymptomatic and underdiagnosed; consequently, there is a demand for simple, non-invasive diagnostic tools. In this study, we developed a method to quantify liver steatosis based on miRNAs, present in liver and serum, that correlate with [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is often asymptomatic and underdiagnosed; consequently, there is a demand for simple, non-invasive diagnostic tools. In this study, we developed a method to quantify liver steatosis based on miRNAs, present in liver and serum, that correlate with liver fat. The miRNAs were analyzed by miRNAseq in liver samples from two cohorts of patients with a precise quantification of liver steatosis. Common miRNAs showing correlation with liver steatosis were validated by RT-qPCR in paired liver and serum samples. Multivariate models were built using partial least squares (PLS) regression to predict the percentage of liver steatosis from serum miRNA levels. Leave-one-out cross validation and external validation were used for model selection and to estimate predictive performance. The miRNAseq results disclosed (a) 144 miRNAs correlating with triglycerides in a set of liver biobank samples (n = 20); and (b) 124 and 102 miRNAs correlating with steatosis by biopsy digital image and MRI analyses, respectively, in liver samples from morbidly obese patients (n = 24). However, only 35 miRNAs were common in both sets of samples. RT-qPCR allowed to validate the correlation of 10 miRNAs in paired liver and serum samples. The development of PLS models to quantitatively predict steatosis demonstrated that the combination of serum miR-145-3p, 122-5p, 143-3p, 500a-5p, and 182-5p provided the lowest root mean square error of cross validation (RMSECV = 1.1, p-value = 0.005). External validation of this model with a cohort of mixed MASLD patients (n = 25) showed a root mean squared error of prediction (RMSEP) of 5.3. In conclusion, it is possible to predict the percentage of hepatic steatosis with a low error rate by quantifying the serum level of five miRNAs using a cost-effective and easy-to-implement RT-qPCR method. Full article
(This article belongs to the Special Issue Liver Damage and Associated Metabolic Disorders)
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Review

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24 pages, 1297 KiB  
Review
The Role of Short-Chain Fatty Acids in Metabolic Dysfunction-Associated Steatotic Liver Disease and Other Metabolic Diseases
by Eliane Münte and Phillipp Hartmann
Biomolecules 2025, 15(4), 469; https://doi.org/10.3390/biom15040469 - 22 Mar 2025
Viewed by 1550
Abstract
With its increasing prevalence, metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major global public health concern over the past few decades. Growing evidence has proposed the microbiota-derived metabolites short-chain fatty acids (SCFAs) as a potential factor in the pathophysiology of [...] Read more.
With its increasing prevalence, metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major global public health concern over the past few decades. Growing evidence has proposed the microbiota-derived metabolites short-chain fatty acids (SCFAs) as a potential factor in the pathophysiology of MASLD and related metabolic conditions, such as obesity and type 2 diabetes mellitus (T2DM). By influencing key pathways involved in energy homeostasis, insulin sensitivity, and inflammation, SCFAs play an important role in gut microbiota composition, intestinal barrier function, immune modulation, and direct metabolic signaling. Furthermore, recent animal and human studies on therapeutic strategies targeting SCFAs demonstrate their potential for treating these metabolic disorders. Full article
(This article belongs to the Special Issue Liver Damage and Associated Metabolic Disorders)
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23 pages, 1077 KiB  
Review
Intestinal-Failure-Associated Liver Disease: Beyond Parenteral Nutrition
by Irene Mignini, Giulia Piccirilli, Federica Di Vincenzo, Carlo Covello, Marco Pizzoferrato, Giorgio Esposto, Linda Galasso, Raffaele Borriello, Maurizio Gabrielli, Maria Elena Ainora, Antonio Gasbarrini and Maria Assunta Zocco
Biomolecules 2025, 15(3), 388; https://doi.org/10.3390/biom15030388 - 8 Mar 2025
Viewed by 1528
Abstract
Short bowel syndrome (SBS), usually resulting from massive small bowel resections or congenital defects, may lead to intestinal failure (IF), requiring intravenous fluids and parenteral nutrition to preserve patients’ nutritional status. Approximately 15% to 40% of subjects with SBS and IF develop chronic [...] Read more.
Short bowel syndrome (SBS), usually resulting from massive small bowel resections or congenital defects, may lead to intestinal failure (IF), requiring intravenous fluids and parenteral nutrition to preserve patients’ nutritional status. Approximately 15% to 40% of subjects with SBS and IF develop chronic hepatic damage during their life, a condition referred to as intestinal-failure-associated liver disease (IFALD), which ranges from steatosis to fibrosis or end-stage liver disease. Parenteral nutrition has been largely pointed out as the main pathogenetic factor for IFALD. However, other elements, such as inflammation, bile acid metabolism, bacterial overgrowth and gut dysbiosis also contribute to the development of liver damage and may deserve specific treatment strategies. Indeed, in our review, we aim to explore IFALD pathogenesis beyond parenteral nutrition. By critically analyzing recent literature, we seek to delve with molecular mechanisms and metabolic pathways underlying liver damage in such a complex set of patients. Full article
(This article belongs to the Special Issue Liver Damage and Associated Metabolic Disorders)
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