Expression of TWEAK/Fn14 axis in the context of metabolic dysfunction associated-fatty liver disease: an approach in liver regeneration

Daniel Romero-Suárez; José Belisario Solana Tinoco; María Cecilia García-Espiñeira; Lina Lambis-Anaya; Amileth Suarez-Causado

doi:10.47892/rgp.2024.443.1718

Authors

Daniel Romero-Suárez Department of Biochemistry, Faculty of Medicine, University of Cartagena, Cartagena de Indias, Colombia. https://orcid.org/0000-0002-6776-6946
José Belisario Solana Tinoco Unit of Liver and Biliary Tract, Department of General and Digestive System Surgery of Caribbean, University Hospital of Cartagena, University of Cartagena, Cartagena de Indias, Colombia. https://orcid.org/0000-0002-3748-2678
Doctora Department of Pathology, Faculty of Medicine, University of Cartagena, Cartagena de Indias, Colombia. https://orcid.org/0000-0002-4120-1533
Lina Lambis-Anaya Department of Biochemistry, Faculty of Medicine, University of Cartagena, Cartagena de Indias, Colombia. https://orcid.org/0000-0002-5894-2530
Doctora Department of Biochemistry, Faculty of Medicine, University of Cartagena, Cartagena de Indias, Colombia. https://orcid.org/0000-0003-2807-0679

DOI:

https://doi.org/10.47892/rgp.2024.443.1718

Keywords:

Fatty liver, TWEAK receptor, Fn14 receptor, Liver regeneration

Abstract

Background: One of the pathways involved in liver regeneration processes is TWEAK/Fn14 (tumor necrosis factor-related weak inducer of apoptosis/fibroblast growth factor-inducible 14), which has been proposed to act directly and selectively on hepatic progenitor cells; however, its role in the regeneration of steatotic liver metabolic dysfunction associated fatty liver disease has not been fully elucidated. Objective: To evaluate the behavior of Fn14 and its ligand TWEAK, as well as cellular stress signals as biochemical cues for possible liver regeneration in MAFLD. Materials and methods: A prospective study was carried out where the behavior of Fn14 and its ligand TWEAK, as well as cellular stress signals were observed as biochemical indications of a possible liver regeneration in a condition of tissue damage caused by excessive lipid accumulation. The expression of TWEAK, Fn14 and heat shock proteins in hepatic steatosis of non-alcoholic origin was assessed using immunohistochemistry and western blotting. Results: The histological classification of the tissues under study corresponded to microvesicular steatosis. We report a high level of expression of heat shock proteins in the cytoplasm. The expression of TWEAK and Fn14 in liver tissue affected by lipid accumulation was localized in the cytoplasm of hepatocytes, showing a higher intensity of reactivity for Fn14 compared to its ligand TWEAK. Conclusion: The expression of TWEAK/Fn14 axis was positive suggesting reactivity of the signaling pathway in metabolic dysfunction associated fatty liver disease.

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