Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10165154 | JACC: Heart Failure | 2015 | 9 Pages |
Abstract
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.
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Authors
Laurent PhD, Ernesto PhD, Maria PhD, Victoria PhD, Elodie Rousseau, J. Rafael MD, Faiez PhD, MD, Patrick PhD, MD, Natalia PhD,