Doxorubicin-induced cardiac dysfunction is ameliorated in galectin-3 knockout mice

SEROPIAN, IGNACIO; FONTANA ESTEVEZ, FLORENCIA S.; VILLAVERDE, ALEJO; BUSTOS, ROMINA; TOUCEDA, VANESSA; SELSER, CAROLINA; CACCIAGIÚ, LEONARDO; CIANCIULLI, TOMÁS; CASSANOVA, VERÓNICA; VIDAL, MARÍA AGUSTINA; MIKSZTOWICZ, VERÓNICA; GONZÁLEZ, GERMÁN E.

Mar del Plata

Encuentro; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2022

Sociedad Argentina de Investigación Clínica

Background: Doxorubicin (DOX) treatment leads to cardiovascular toxicity through a direct effect on cardiomyocytes and inflammation. Objective: We aimed to study the role of Galectin-3 (Gal3) in DOX-induced cardiac toxicity. Methods: Male C57 (N=30) and Gal- 3KO (N=32) mice with a single dose administration of DOX (15 mg/ kg, IP) or saline solution (S) (0.2 ml, IP). Serum creatine phosphokinase (CPK) at 3 days was measure for cardiac damage. Cardiac remodeling and function studied in vivo by echocardiography (echo) (n=10/group) and catheterization at 7 days (n=5/group). Cardiac fibrosis (%) was measured in picrosirius red-stained sections. Results are shown as Mean±SEM. p