RT Journal Article
T1 The detrimental role of galectin‐3 and endoplasmic reticulum stress in the cardiac consequences of myocardial ischemia in the context of obesity
A1 Jiménez González, Sara
A1 Delgado Valero, Beatriz
A1 Islas, Fabian
A1 Romero Miranda, Ana
A1 Luaces Méndez, María
A1 Ramchandani, Bunty
A1 Cuesta Corral, María
A1 Montoro Garrido, Alejandro
A1 Martínez Martínez, Ernesto
A1 Cachofeiro Ramos, María Victoria
AB The association between cardiac fibrosis and galectin-3 was evaluated in patients with acute myocardial infarction (MI). The role of galectin-3 and its association with endoplasmic reticulum (ER) stress activation in the progression of cardiovascular fibrosis was also evaluated in obese-infarcted rats. The inhibitor of galectin-3 activity, modified citrus pectin (MCP; 100 mg/kg/day), and the inhibitor of the ER stress activation, 4-phenylbutyric acid (4-PBA; 500 mg/kg/day), were administered for 4 weeks after MI in obese rats. Overweight-obese patients who suffered a first MI showed higher circulating galectin-3 levels, higher extracellular volume, and LV infarcted size, as well as lower E/e'ratio and LVEF compared with normal-weight patients. A correlation was observed between galectin-3 levels and extracellular volume. Obese-infarcted animals presented cardiac hypertrophy and reduction in LVEF, and E/A ratio as compared with control animals. They also showed an increase in galectin-3 gene expression, as well as cardiac fibrosis and reduced autophagic flux. These alterations were associated with ER stress activation characterized by enhanced cardiac levels of binding immunoglobulin protein, which were correlated with those of galectin-3. Both MCP and 4-PBA not only reduced cardiac fibrosis, oxidative stress, galectin-3 levels, and ER stress activation, but also prevented cardiac functional alterations and ameliorated autophagic flux. These results show the relevant role of galectin-3 in the development of diffuse fibrosis associated with MI in the context of obesity in both the animal model and patients. Galectin-3 in tandem with ER stress activation could modulate different downstream mechanisms, including inflammation, oxidative stress, and autophagy.
PB Wiley
SN 0892-6638
SN 1530-6860
YR 2024
FD 2024-07-31
LK https://hdl.handle.net/20.500.14352/112740
UL https://hdl.handle.net/20.500.14352/112740
LA eng
NO Jiménez-González S, Delgado-Valero B, Islas F, Romero-Miranda A, Luaces M, Ramchandani B, Cuesta-Corral M, Montoro-Garrido A, Martínez-Martínez E, Cachofeiro V. The  detrimental role of galectin-3 and endoplasmic reticulum stress in the cardiac consequences of myocardial ischemia in the context of obesity. J. FASEB J. 2024 Jul 31;38(14):e23818.
NO Instituto de Salud Carlos III
NO Unión Europea
DS Docta Complutense
RD 9 abr 2025