Galectin-3 is a member of the galectin family, which are β‑galactoside‑binding lectins with ≥1 evolutionary conserved carbohydrate‑recognition domain. It binds proteins in a carbohydrate‑dependent and ‑independent manner. Galectin‑3 is predominantly located in the cytoplasm; however, it shuttles into the nucleus and is secreted onto the cell surface and into biological fluids including serum and urine. It serves important functions in numerous biological activities including cell growth, apoptosis, pre‑mRNA splicing, differentiation, transformation, angiogenesis, inflammation, fibrosis and host defense. Numerous previous studies have indicated that galectin‑3 may be used as a diagnostic or prognostic biomarker for certain types of heart disease, kidney disease and cancer. With emerging evidence to support the function and application of galectin‑3, the current review aims to summarize the latest literature regarding the biomarker characteristics and potential therapeutic application of galectin‑3 in associated diseases.

/pdf/galectin-3-as-a-novel-biomarker-for-disease-diagnosis-and-a-5ci70sx8cb.pdf

Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review)

The cardiac extracellular matrix (ECM) fills the space between cells, supports tissue organization, and transduces mechanical, chemical, and biological signals to regulate homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role in cardiac repair. A balanced turnover of ECM through regulation of synthesis by myofibroblasts and degradation by matrix metalloproteinases (MMPs) is critical for proper scar formation. In this review, we summarize the current literature on the roles of myofibroblasts, MMPs, and ECM proteins in MI-induced LV remodeling. In addition, we discuss future research directions that are needed to further elucidate the molecular mechanisms of ECM actions to optimize cardiac repair.

/pdf/myofibroblasts-and-the-extracellular-matrix-network-in-post-57e4h3y2p1.pdf

Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling

Objective— Galectin-3 (Gal-3) can affect atherogenesis by multiple mechanisms, but it remains scarcely known whether plasma Gal-3 levels predict cardiovascular events in patients with coronary artery disease. Therefore, we investigated if Gal-3 predicts cardiovascular death in patients with coronary artery disease of the Genetic and ENvironmental factors In Coronary Artery disease study. Approach and Results— In a prospective cohort study, we measured the plasma levels of Gal-3 in 1013 randomly selected patients who underwent coronary angiography and long-term follow-up to assess incident cardiovascular events. The primary end points were (1) cardiovascular death and (2) a composite of cardiovascular death, acute coronary syndrome, and stroke. Secondary end points entailed (1) acute myocardial infarction, (2) stroke, and (3) a composite fatal ischemic event including fatal myocardial infarction and stroke. The effect of Gal-3 on prognosis was assessed using Kaplan–Meier analysis and multivariate Cox’s regression. During long-term follow-up (median, 7.2 years), 115 cardiovascular deaths occurred (15.2%), more commonly in the high Gal-3 tertile (25.2%) than in the intermediate and the low tertiles (13.6% versus 7.5%, respectively; P P =0.020) along with age, left ventricular ejection fraction, and coronary atherosclerotic burden. Conclusions— In high cardiovascular risk patients referred for coronary angiography Gal-3 is a strong independent predictor of cardiovascular death.

Galectin-3 Predicts Long-Term Cardiovascular Death in High-Risk Patients With Coronary Artery Disease

Atherosclerosis is a multifactorial chronic inflammatory arterial disease forming the pathological basis of many cardiovascular diseases such as coronary heart disease, heart failure, and stroke. Numerous studies have implicated inflammation as a key player in the initiation and progression of atherosclerosis. Galectin-3 (Gal-3) is a 30 kDa β-galactose, highly conserved and widely distributed intracellularly and extracellularly. Gal-3 has been demonstrated in recent years to be a novel inflammatory factor participating in the process of intravascular inflammation, lipid endocytosis, macrophage activation, cellular proliferation, monocyte chemotaxis, and cell adhesion. This review focuses on the role of Gal-3 in atherosclerosis and the mechanism involved and several classical Gal-3 agonists and antagonists in the current studies.

/pdf/galectin-3-is-a-potential-mediator-for-atherosclerosis-1kr05m9wt8.pdf

Galectin-3 Is a Potential Mediator for Atherosclerosis.

Galectin-3 and post-myocardial infarction cardiac remodeling

Background: Galectin-3, a biomarker associated with fibrosis and inflammation, has been implicated in development and progression of heart failure (HF) and predicts increased mortality and morbidity in this condition. HF frequently develops after myocardial infarction (MI), contributing to worse outcome. The aim of this study is to assess the association between galectin-3 levels and various clinical parameters in acute phase of first MI treated with primary percutaneous coronary intervention (pPCI) in patients without prior HF. Methods: We included 145 consecutive patients with first acute MI treated with pPCI with stent implantation. Exclusion criteria were: prior HF, severe valvular diseases, coexisting cancers, connective tissue diseases and cirrhosis. Serum galectin-3 concentration was measured within 3–5 days after onset of acute MI.Results: Thirty-six patients with the highest galectin-3 levels (4th quartile, > 16 ng/mL) were compared to 109 subjects with a biomarker concentration ≤ 16 ng/mL. Elevated galectin-3 levels were more often observed in females, the elderly, subjects with coexisting diabetes, renaldysfunction and permanent atrial fi brillation (AF). Galectin-3 correlated with N-terminal pro-B-type natriuretic peptide (r = 0.27, p 16 ng/mL. Conclusions: Elevated galectin-3 levels were associated with a higher rate of new-onset AF and diuretics treatment during hospitalization in patients with first MI treated with pPCI without prior HF.

/pdf/the-association-between-galectin-3-and-clinical-parameters-4n6r0mgca9.pdf

The association between galectin-3 and clinical parameters in patients with first acute myocardial infarction treated with primary percutaneous coronary angioplasty.

Introduction Soluble urokinase plasminogen activator receptor (suPAR) level reflects the general condition of the organism and was proved to give independent information in risk stratification of patients. The aim of this study was to assess the usefulness of suPAR in the prediction of adverse cardiac events in patients with first myocardial infarction (MI) undergoing primary percutaneous coronary intervention. Additionally, the diagnostic power of suPAR was assessed. Material and methods One hundred and thirty-nine of 150 consecutive patients were included in the study. Serum suPAR level (ELISA, Virogates) as well as C-reactive protein (on admission and at discharge) and maximum troponin T (assessed from successive 6-hour periods of blood collection) were measured. In the 1-year follow-up study the following major adverse cardiac events were observed: myocardial infarction, revascularization, stroke and death. Results Multi-variable analysis revealed prognostic usefulness only for suPAR and glomerular filtration rate: p < 0.0001 and p = 0.018; OR = 2.59 and OR = 0.98 respectively, with area under the curve in receiver operating characteristic analysis for both parameters simultaneously 0.89 (p < 0.0001). There was no correlation between suPAR level and the left ventricular dysfunction parameters or the MI type. Conclusions Soluble urokinase plasminogen activator receptor level appears to be an independent useful biomarker for the prediction of major adverse cardiac events early after first myocardial infarction. The biomarker's level seems to have more prognostic than diagnostic power.

https://www.termedia.pl/Journal/-19/pdf-28677-10?filename=soluble urokinase.pdf

Soluble urokinase plasminogen activator receptor in one-year prediction of major adverse cardiac events in patients after first myocardial infarction treated with primary percutaneous coronary intervention.

Context: Galectin-3, as a biomarker of inflammation and fibrosis, has been reported to be associated with coronary artery disease.Objective: The study aimed to assess the relationship between galectin-3 levels and the occurrence of reinfarction early after myocardial infarction (MI).Methods: The study included 145 consecutive patients with first MI treated invasively. Serum galectin-3 was measured using VIDAS (bioMerieux, Marcy-l'Etoile, France).Results: The independent predictors of reinfarction in our group were as follows: female gender, elevated hs-C-reactive protein and galectin-3 levels (measured both at discharge).Conclusions: Galectin-3 might be an additional useful biomarker in prediction for reinfarction early after first MI.

The association between galectin-3 and occurrence of reinfarction early after first myocardial infarction treated invasively

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The association between galectin-3 and clinical parameters in patients with first acute myocardial infarction treated with primary percutaneous coronary angioplasty.

Soluble urokinase plasminogen activator receptor in one-year prediction of major adverse cardiac events in patients after first myocardial infarction treated with primary percutaneous coronary intervention.

The association between galectin-3 and occurrence of reinfarction early after first myocardial infarction treated invasively