Calvier, LaurentMartínez Martínez, ErnestoMiana, MaríaCachofeiro Ramos, María VictoriaRousseau, ElodieSábada, J. RafaelZannad, FaiezRossignol, PatrickLópez Andrés, Natalia2025-01-302025-01-302015-01-03Calvier, L., Martinez-Martinez, E., Miana, M., Cachofeiro, V., Rousseau, E., Sádaba, J. R., Zannad, F., Rossignol, P., & López-Andrés, N. (2015). The impact of galectin-3 inhibition on aldosterone-induced cardiac and renal injuries. JACC. Heart failure, 3(1), 59–67. https://doi.org/10.1016/j.jchf.2014.08.0022213-177910.1016/j.jchf.2014.08.002https://hdl.handle.net/20.500.14352/117092Objectives: This study investigated whether galectin (Gal)-3 inhibition could block aldosterone-induced cardiac and renal fibrosis and improve cardiorenal dysfunction. Background: Aldosterone is involved in cardiac and renal fibrosis that is associated with the development of cardiorenal injury. However, the mechanisms of these interactions remain unclear. Gal-3, a β-galactoside-binding lectin, is increased in heart failure and kidney injury. Methods: Rats were treated with aldosterone-salt combined with spironolactone (a mineralocorticoid receptor antagonist) or modified citrus pectin (a Gal-3 inhibitor), for 3 weeks. Wild-type and Gal-3 knockout mice were treated with aldosterone for 3 weeks. Hemodynamic, cardiac, and renal parameters were analyzed. Results: Hypertensive aldosterone-salt-treated rats presented cardiac and renal hypertrophy (at morphometric, cellular, and molecular levels) and dysfunction. Cardiac and renal expressions of Gal-3 as well as levels of molecular markers attesting fibrosis were also augmented by aldosterone-salt treatment. Spironolactone or modified citrus pectin treatment reversed all of these effects. In wild-type mice, aldosterone did not alter blood pressure levels but increased cardiac and renal Gal-3 expression, fibrosis, and renal epithelial-mesenchymal transition. Gal-3 knockout mice were resistant to aldosterone effects. Conclusions: In experimental hyperaldosteronism, the increase in Gal-3 expression was associated with cardiac and renal fibrosis and dysfunction but was prevented by pharmacological inhibition (modified citrus pectin) or genetic disruption of Gal-3. These data suggest a key role for Gal-3 in cardiorenal remodeling and dysfunction induced by aldosterone. Gal-3 could be used as a new biotarget for specific pharmacological interventions.engjournal articlehttps://doi.org/10.1016/j.jchf.2014.08.00225458174https://www.sciencedirect.com/science/article/pii/S2213177914003886?via%3Dihubrestricted access612aldosteronebiomarkercardiorenal injurycollagengalectin-3Sistema cardiovascular24 Ciencias de la Vida