ArticleACS pharmacology & translational science2026
Hepatic Overexpression of a Novel Soluble Endogenous Transforming Growth Factor β Type II Receptor-Immunoglobulin G1 Fc Fusion Protein (TβRII-SE/Fc) Attenuates Early Stage Metabolic Dysfunction-Associated Steatotic Liver Disease in Rats.
Article in ACS pharmacology & translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease. Due to its complex pathophysiology, treatment options remain limited. Transforming growth factor β (TGF-β) is a pleiotropic cytokine involved in the regulation of liver fibrosis and metabolism. Previously, we have demonstrated the antifibrotic effect of TβRII-SE/Fc delivered by a lentiviral vector (Lv) in a liver fibrosis model. TβRII-SE/Fc is a fusion protein composed of the soluble isoform of the TGF-β type II receptor (TβRII-SE) and the human IgG-Fc domain. In this study, we evaluated the potential of TβRII-SE/Fc to attenuate key metabolic and hepatic features in an early stage MASLD model using lentiviral-mediated hepatic overexpression. We studied the effect of intrahepatic administration of Lv.TβRII-SE/Fc in a rat MASLD model induced by a Western diet. To achieve that, body composition-related parameters, biochemical, histological, ultrastructural, and RT-qPCR analyses were performed. Intrahepatic delivery of Lv.TβRII-SE/Fc is associated with improvements in several features of MASLD: (i) Attenuated liver microvesicular steatosis. (ii) Reduced liver fibrosis, together with decreased IL-6 and TGF-β2 gene expression. (iii) Changes in the expression of genes associated with free fatty acid (FFA) utilization, uptake, and
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