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oai:docta.ucm.es:20.500.14352/1158392025-01-24T00:48:01Zcom_20.500.14352_14col_20.500.14352_15

Martínez Martínez, Ernesto Calvier L, Fernández-Celis A, Rousseau E Jurado-López R Rossoni LV Jaisser F Zannad F Rossignol P, Cachofeiro Ramos, María Victoria López-Andrés N 2025-01-23T12:37:56Z 2025-01-23T12:37:56Z 2015-10-01 Martínez-Martínez E, Calvier L, Fernández-Celis A, Rousseau E, Jurado-López R, Rossoni LV, Jaisser F, Zannad F, Rossignol P, Cachofeiro V, López-Andrés N. Galectin-3 blockade inhibits cardiac inflammation and fibrosis in experimental hyperaldosteronism and hypertension. Hypertension. 2015 Oct;66(4):767-75. doi: 10.1161/HYPERTENSIONAHA.115.05876. Epub 2015 Aug 3. PMID: 26238446. 10.1161/HYPERTENSIONAHA.115.05876 https://hdl.handle.net/20.500.14352/115839 0194-911X https://doi.org/10.1161/HYPERTENSIONAHA.115.05876 26238446 https://pubmed.ncbi.nlm.nih.gov/26238446/ https://www.ahajournals.org/doi/10.1161/hypertensionaha.115.05876 Hypertensive cardiac remodeling is accompanied by molecular inflammation and fibrosis, 2 mechanisms that finally affect cardiac function. At cardiac level, aldosterone promotes inflammation and fibrosis, although the precise mechanisms are still unclear. Galectin-3 (Gal-3), a β-galactoside-binding lectin, is associated with inflammation and fibrosis in the cardiovascular system. We herein investigated whether Gal-3 inhibition could block aldosterone-induced cardiac inflammation and fibrosis and its potential role in cardiac damage associated with hypertension. Aldosterone-salt-treated rats presented hypertension, cardiac inflammation, and fibrosis that were prevented by the pharmacological inhibition of Gal-3 with modified citrus pectin. Cardiac inflammation and fibrosis presented in spontaneously hypertensive rats were prevented by modified citrus pectin treatment, whereas Gal-3 blockade did not modify blood pressure levels. In the absence of blood pressure modifications, Gal-3 knockout mice were resistant to aldosterone-induced cardiac inflammation. In human cardiac fibroblasts, aldosterone increased Gal-3 expression via its mineralocorticoid receptor. Gal-3 and aldosterone enhanced proinflammatory and profibrotic markers, as well as metalloproteinase activities in human cardiac fibroblasts, effects that were not observed in Gal-3-silenced cells treated with aldosterone. In experimental hyperaldosteronism, the increase in Gal-3 expression was associated with cardiac inflammation and fibrosis, alterations that were prevented by Gal-3 blockade independently of blood pressure levels. These data suggest that Gal-3 could be a new molecular mechanism linking cardiac inflammation and fibrosis in situations with high-aldosterone levels, such as hypertension. eng restricted access Galectin-3 blockade inhibits cardiac inflammation and fibrosis in experimental hyperaldosteronism and hypertension. Hypertension journal article