Molecular Mechanisms of Fibrosis in Chronic Liver Diseases

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 1 June 2026 | Viewed by 16

Special Issue Editors


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Guest Editor
The Liver Institute, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel
Interests: metabolic dysfunction-associated steatohepatitis (MASH); liver fibrosis; natural killer (NK) cells; hepatic stellate cells (HSCs); NK-HSCs interplay; gut–liver axis; antifibrotic therapies

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Guest Editor
Department of Pediatrics, Medical Center and Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem 9190501, Israel
Interests: extracellular vesicles (EVs); microvesicels; exosomes; cell–cell communication; hepatic stellate cells (HSCs); miRNAs

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Guest Editor
Department of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem 9190501, Israel
Interests: epigenetic regulation (especially DNA methylation, during intestinal development, inflammation, and tumorigenesis); early-life epigenetic programming effects on tissue remodeling and disease susceptibility

Special Issue Information

Dear Colleagues,

Liver fibrosis is a dynamic pathological process marked by excessive extracellular matrix (ECM) accumulation in response to chronic liver injury. It commonly arises from metabolic dysfunction-associated steatohepatitis (MASH), viral hepatitis, alcohol misuse, and autoimmune or cholestatic liver diseases. At the molecular level, fibrosis is mediated by the sustained activation of hepatic stellate cells (HSCs), which transdifferentiate into myofibroblast-like cells that secrete collagenous and non-collagenous ECM proteins, leading to progressive disruption of liver structure and function.

The progression of liver fibrosis is governed by complex interactions involving cytokine signaling, immune cell crosstalk, oxidative stress, and metabolic reprogramming. Recent research highlights the crucial roles of immune–metabolic pathways, gut–liver axis dysregulation, and epigenetic modifications in modulating fibrogenic activity. Emerging technologies, such as single-cell transcriptomics and spatial omics, are further unraveling the heterogeneity and regulatory networks within the fibrotic liver microenvironment.

This Special Issue aims to explore the molecular mechanisms underlying hepatic fibrosis and their translational implications. We welcome original research articles, reviews, and perspectives that provide insights into fibrosis biology, biomarker discovery, and antifibrotic therapies. We look forward to your valuable contributions.

Dr. Ahmad Salhab
Dr. Regina Golan-Gerstl
Dr. Ihab Ansari
Guest Editors

Manuscript Submission Information

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Keywords

  • liver fibrosis
  • MASH
  • immune checkpoints
  • epigenetic regulation
  • hepatic stellate cells (HSCs)
  • antifibrotic therapy
  • molecular mechanisms
  • inflammation
  • ROS

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Published Papers

This special issue is now open for submission.
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