Exploration of Drug Targets for Liver Fibrosis Based on Hepatic Stellate Cells and Extracellular Matrix Remodeling

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

Deadline for manuscript submissions: 31 July 2026 | Viewed by 3

Special Issue Editor


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Guest Editor
Department of Pharmacology, University of Valencia, avda. Blasco Ibañez n.15, 46010 Valencia, Spain
Interests: antiretroviral therapy; hepatic diseases; liver fibrosis; mitochondria; autophagy; mitochondrial dysfunction and its role in pathogenesis; cellular mechanisms involved in the toxicity of antiretroviral drugs and HIV, with special focus on mitochondrial function; endoplasmic reticular stress and activation of survival programs (autophagy) and cellular death (apoptosis)
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Dear Colleagues,

Liver fibrosis (LF) is a pathological wound-healing response manifested through the excessive buildup of extracellular matrix (ECM) in the liver as a result of prolonged inflammation and injury. It is the common denominator of most types of chronic liver disease caused by different etiologies (alcohol consumption, viral hepatitis, and steatosis related to metabolic dysfunction being the most common). If it progresses, LF can lead to severe, irreversible damage called cirrhosis, causing liver failure, portal hypertension with its complications (ascites, jaundice, and bleeding), and the development of HCC (hepatocellular carcinoma). Activation of hepatic stellate cells (HSCs) into a myofibroblast phenotype represents a key event in LF, as these cells are the primary source of ECM. Of note, although improved management of the underlying diseases can halt progression and, to an extent, even reverse LF, there are currently no specific approved antifibrotic therapies. Recent research has focused on HSCs and, specifically, ECM remodeling as therapeutic targets.

Prof. Dr. Nadezda Apostolova
Guest Editor

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Keywords

  • liver fibrosis
  • collagen
  • hepatic stellate cells
  • senescence
  • animal models
  • extracellular matrix
  • hepatitis
  • cytokines
  • biomarkers
  • MASH
  • MASLD
  • cirrhosis
  • hepatocellular carcinoma

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