Galectin-3
المؤلف:
Marcello Ciaccio
المصدر:
Clinical and Laboratory Medicine Textbook 2021
الجزء والصفحة:
p303-304
2025-09-06
386
Galectin-3 is a lectin that binds compounds containing a β-galactosidic bond, characteristic of many glycans on the cell surface. Many experimental studies show that galectin-3 is involved in many functions at the cellular level, such as adhesion, activation, chemotactic attraction, growth, differentiation, and apoptosis. An increase in galectin-3 expression induces fibroblast proliferation and collagen production, thus contributing to the increase in cardiac fibrosis and sub sequent remodeling.
Especially after the first decade of this century, numerous clinical studies on this biomarker have been published, favored by the commercialization of immunometric methods applied to automated platforms with excellent analytical performance. Galectin-3 was initially studied as a mediator of growth and progression of several types of tumors, and only later, its strong association with clinical conditions characterized by chronic inflammation and interstitial fibrosis was noted. Galectin-3 is present in the cytoplasm of different cell types and is particularly abundant in macrophages.
The rationale for the candidacy of galectin-3 as a marker in heart failure comes from studies in animal models published in the early years of the new century, which have shown that this leptin can regulate the hypertrophic response and functional cardiac damage following the administration of angiotensin II or constriction of the aorta. The results of these experimental studies paved the way for clinical trials that sought to evaluate whether galectin-3 could play a role as a marker of fibrosis, inflammation, and cardiac remodeling in patients with heart failure. Furthermore, in November 2010, the Food and Drug Administration (FDA) approved the determination of galectin-3 in conjunction with clinical evaluation to define the prognosis of patients with chronic heart failure. Subsequently, many studies have been published to assess the prognostic relevance of galectin-3 in patients with heart failure, especially HFpEF type. Unfortunately, these studies are primarily case–control. In 2015, a meta-analysis, considering 9 cohort studies, showed a significant association between mortality and bio marker levels; however, this study has, as an important limitation related to the significant heterogeneity of the data used for the meta- analysis. In addition, data derived from cohort studies are generally the result of post hoc analysis and, therefore, require confirmation with specific clinical protocols.
As previously pointed out for markers of inflammation and turnover of collagen and extracellular matrix, also for galectin-3 a modest difference is observed between the concentrations of healthy subjects and heart failure patients (on average from 15% to 40%). For this reason, in many statistical evaluations, the measurement of galectin-3 does not add significant prognostic information to other prognostic markers (especially that of natriuretic peptides).
It should be noted, however, that the biological variability of galectin-3 both intraindividually (about 5–8% in healthy subjects, as well as in patients with chronic stable heart failure) and interindividually (about 27% in healthy subjects and 40% in patients with chronic stable heart failure) is much lower than that of natriuretic peptides or troponins. The relatively low biological variability coupled with the excellent analytical performance of the currently available automated assay methods makes the biochemical information provided by galectin-3 very robust in monitoring individual subjects/ patients.
Compared with the sST2 protein, galectin-3 possesses the advantage of being more closely related to chronic inflammatory processes resulting in interstitial fibrosis in patients with heart failure. If this hypothesis is confirmed, galectin-3 could be considered a biomarker of cardiac remodeling associated with myocardial interstitial fibrosis. Thus, Galectin-3 could be used to screen patients with HFpEF who are still asymptomatic or pauci-asymptomatic, to identify those who will need to undergo more expensive (such as gadolinium- enhanced MRI) or invasive (such as biopsy or arteriography) tests to confirm cardiac fibrosis, and then be targeted to specific and more aggressive therapies.
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