2016
DOI: 10.1093/ecco-jcc/jjw013
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Galectin-3 Plays an Important Pro-inflammatory Role in the Induction Phase of Acute Colitis by Promoting Activation of NLRP3 Inflammasome and Production of IL-1β in Macrophages

Abstract: Gal-3 expression promotes acute DSS-induced colitis and plays an important pro-inflammatory role in the induction phase of colitis by promoting the activation of NLRP3 inflammasome and production of IL-1β in macrophages.

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Cited by 102 publications
(68 citation statements)
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“…Human Gal‐3 is a chimera‐type β‐galactoside‐binding galectin protein that exerts physiological effects through carbohydrate‐recognition domains and is mainly secreted by cardiac myocytes and inflammatory cells . As Gal‐3 level had been reported increases with reducing eGFR independent of cardiovascular complications (for example heart failure), and also elevated in patients with activated inflammation . CRP and BMI has also been reported associated with Gal‐3 level, however we did not found the correlation in our cohort.…”
Section: Discussioncontrasting
confidence: 60%
“…Human Gal‐3 is a chimera‐type β‐galactoside‐binding galectin protein that exerts physiological effects through carbohydrate‐recognition domains and is mainly secreted by cardiac myocytes and inflammatory cells . As Gal‐3 level had been reported increases with reducing eGFR independent of cardiovascular complications (for example heart failure), and also elevated in patients with activated inflammation . CRP and BMI has also been reported associated with Gal‐3 level, however we did not found the correlation in our cohort.…”
Section: Discussioncontrasting
confidence: 60%
“…Although further studies with larger sample size are needed to confirm this conclusion, it is possible that the increase in serum galectins might represent an early event in the inflammatory cascade and not subsequently rise further with increase of disease activity. The recent reports showing that several galectin members play key pathogenic roles in animal models of colitis [27] and galectin-3 caused macrophage activation in the induction phase of colitis in a dextran sodium sulphate animal model of colitis [28] are in line with this possibility. The increased level of serum galectin-3 in IBD patients found in this study is in agreement with an early report showing higher serum galectin-3 level in IBD patients, irrespective of their disease activity, compared with healthy people [22].…”
Section: Discussionmentioning
confidence: 65%
“…It plays key roles in physiological and pathological processes such as inflammation and fibrosis, which are involved in the development of pulmonary arterial remodeling and stiffness. Gal‐3 is expressed in fibroblasts, endothelial cells, and inflammatory cells such as macrophages, which are associated with cardiac dysfunction through the induction of cardiac fibroblast proliferation, collagen deposition, and ventricular dysfunction . Gal‐3 also promotes vascular damage and cardiovascular fibrosis …”
Section: Introductionmentioning
confidence: 99%