RT Journal Article
T1 The impact of galectin-3 inhibition on aldosterone-induced cardiac and renal injuries
A1 Calvier, Laurent
A1 Martínez Martínez, Ernesto
A1 Miana, María
A1 Cachofeiro Ramos, María Victoria
A1 Rousseau, Elodie
A1 Sábada, J. Rafael
A1 Zannad, Faiez
A1 Rossignol, Patrick
A1 López Andrés, Natalia
AB Objectives: 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.
PB Elsevier
SN 2213-1779
YR 2015
FD 2015-01-03
LK https://hdl.handle.net/20.500.14352/117092
UL https://hdl.handle.net/20.500.14352/117092
LA eng
NO Calvier, 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.2014.08.002
DS Docta Complutense
RD 8 abr 2025