Advances in Genetic/Epigenetic Mechanisms and Biomarker Discovery of Liver Fibrosis

Deadline for manuscript submissions: 31 December 2026.

Guest Editor (1)

Ralf  Weiskirchen
Prof. Ralf Weiskirchen 
Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry (IFMPEGKC), RWTH University Hospital Aachen, Aachen, 52074, Germany
Interests: Liver Disease; Fibrosis; Biomarker; Cytokines; Chemokines; Translational medicine

Special Issue Information

Liver fibrosis, the common pathological response to chronic liver injury, remains a major global health burden leading to cirrhosis and liver failure. While significant progress has been made, a comprehensive understanding of its individual genetic susceptibility, dynamic epigenetic regulation, and reliable biomarkers for early detection and monitoring is still evolving.

We invite the submission of original research articles, comprehensive reviews, short communications, and perspectives that address, but are not limited to, the following key themes:
  • Genetic Architecture: Identification of novel genetic variants, polymorphisms, and heritable factors that influence susceptibility, progression rate, and treatment response in liver fibrosis (e.g., related to metabolic dysfunction-associated steatotic liver disease (MASLD), viral hepatitis, alcoholic liver disease).
  • Epigenetic Drivers: Investigations into DNA methylation, histone modifications, non-coding RNAs (miRNAs, lncRNAs), and other epigenetic mechanisms that regulate the activation of hepatic stellate cells (HSCs), immune cell responses, and the fibrogenic cascade.
  • Biomarker Discovery & Validation: Discovery and rigorous validation of novel non-invasive biomarkers (from blood, imaging, or other biofluids) for the early diagnosis, accurate staging, prognosis prediction, and monitoring of therapeutic efficacy in liver fibrosis.
  • Translational & Clinical Applications: Research on the development of epigenetic therapies, genetic risk stratification tools, and the integration of biomarker panels into clinical decision-making pathways for personalized patient care.

Published Papers (1 Papers)

Open Access

Review

01 July 2026

Organoid Models of Liver Fibrosis: Bridging Genetic and Epigenetic Mechanisms with Biomarker Discovery

Fibrosis is a pathological process characterized by excessive deposition of extracellular matrix, progressive tissue stiffening, and ultimately organ dysfunction. It represents a common endpoint of chronic injury in multiple organs, including the liver, lung, kidney, and heart, and contributes substantially to global morbidity and mortality. Increasing evidence indicates that genetic susceptibility and dynamic epigenetic regulation play important roles in determining individual responses to chronic injury and in shaping fibrogenic signaling pathways. Despite its clinical significance, effective therapies remain limited, partly due to an incomplete understanding of the complex cellular interactions and molecular mechanisms that drive fibrotic disease. Traditional experimental models, including two-dimensional cell cultures and animal systems, often fail to fully recapitulate human tissue architecture and disease complexity. Organoid technology has emerged as a promising platform for modeling human diseases in vitro. Organoids are three-dimensional multicellular structures derived from stem cells or primary tissues that self-organize to mimic key structural and functional aspects of native organs while preserving important genetic and epigenetic characteristics of the originating tissue. Recent advances have enabled the development of organoid-based models that capture critical features of fibrosis, including epithelial injury, fibroblast activation, and extracellular matrix remodeling. These systems provide powerful experimental platforms for investigating molecular mechanisms of fibrosis, studying the influence of genetic and epigenetic regulatory networks, and identifying candidate biomarkers associated with disease progression. This review summarizes current progress in the use of organoid systems to study fibrosis across different organs. The advantages and limitations of these models are discussed, and emerging technologies that may enhance their physiological relevance and utility for biomarker discovery and anti-fibrotic drug development are highlighted.

Ralf Weiskirchen*
Fibrosis
2026,
4
(3), 10011; 
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