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. 2021 Sep 10;9:690397. doi: 10.3389/fcell.2021.690397

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Copyright © 2021 Bertolio, La Colla, Carrea, Romo, Canziani, Echarte, Campisano, Barletta, Monzon, Rodríguez, Chisari and Dewey.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TβRII-SE/Fc overexpression prevents CCl₄-induced liver damage development. (A) Experimental design including lentiviral vector and CCl₄ administrations. Animals were euthanized by CO₂ inhalation after 72 h of the last CCl₄ injection. (B) Representative images of liver gross appearance corresponding to rats treated with vehicle, CCl₄, Lv.TβRII-Fc + CCl_4, and Lv.TβRII-SE/Fc + CCl₄. (C) Percentage (%) of both body weight gain (left panel) and (D) liver-to-body weight ratio (LW/BW) (right panel) of animals in the different experimental groups. *p < 0.05, Vehicle vs. CCl₄, or CCl₄ vs. Lv.TβRII-SE/Fc + CCl₄. (E) Serum activity levels of liver enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the different experimental groups. Results are expressed as IU/L. *p < 0.05, Vehicle vs. CCl₄, or CCl₄ vs. Lv.TβRII-SE/Fc + CCl₄. IU: International units.