Serum Galectin-3 Research Articles

High Serum Galectin-3 Level as a Potential Biomarker of Peripheral Artery Disease in Patients Undergoing Hemodialysis.

Galectin-3 is implicated in the pathogenesis of inflammation and atherosclerosis. Peripheral arterial disease (PAD), characterized by a reduced ankle-brachial index (ABI), is a prognostic marker for mortality in patients on hemodialysis. We investigated the relationship between serum galectin-3 levels and PAD in patients undergoing regular hemodialysis. We carried out a cross-sectional study at a medical center, involving 92 participants. Serum galectin-3 levels were assessed by a commercially available enzyme-linked immunosorbent assay. ABI measurement was done with an automatic device based on oscillometry. Participants were categorized into two groups, normal and low ABI, based on a 0.9 cut-off point. Eighteen patients (19.6%) exhibited a low ABI. In individuals with low ABIs, we observed a greater prevalence of diabetes mellitus, elevated serum C-reactive protein (CRP) levels, increased galectin-3 levels, and lower serum creatinine levels. Furthermore, serum galectin-3 levels (odds ratio [OR]: 1.056, 95% confidence interval [CI]: 1.003-1.112, p = 0.037) and CRP (per 0.1 mg/dL increment, OR: 1.195, 95% CI: 1.032-1.383, p = 0.017) were identified as independent predictors of PAD. Serum galectin-3 and log-transformed CRP levels were also independently and significantly negatively correlated with the left and right ABI values. Serum galectin-3 levels correlate with PAD in patients undergoing maintenance hemodialysis.

Diagnostic Value of Galectin-3 in Exacerbations of Chronic Obstructive Pulmonary Disease.

Background and Objectives: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by acute exacerbations. Systemic inflammation and oxidative stress play an important role in the pathogenesis of COPD. Exacerbations in COPD reduce the quality of life and are associated with rapid disease progression. Galectin-3 is a beta-galactoside-binding lectin of approximately 30 kDa with pro-inflammatory and pro-fibrotic properties. This study aims to analyze the efficacy of serum galectin-3 in predicting exacerbations in COPD patients. Materials and Methods: Baseline demographic and clinical characteristics of all patients were recorded and blood samples were collected. A total of 58 consecutive COPD patients, including 28 patients (19 male and 9 female) with stable COPD and 30 patients (23 male and 7 female) with acute exacerbation of COPD (AECOPD), were included in the study. Results: Serum galectin-3 levels were significantly higher in the AECOPD group compared to the stable COPD group. A logistic regression analysis revealed that increased galectin-3 levels and disease duration were independent predictors of COPD exacerbation (OR = 5.322, 95% CI: 1.178-24.052, p = 0.03; and OR = 1.297, 95% CI: 1.028-1.635, p = 0.028; respectively). Conclusions: The results of our study demonstrated that Galectin-3 was a strong and independent predictor of exacerbations in COPD patients.

Association of serum galectin-3 levels with mortality and cardiovascular disease outcomes in hemodialysis patients: a systematic review and dose–response meta-analysis

BackgroundGalectin-3 has been proposed as a candidate marker for cardiovascular risk stratification, although its role in kidney failure is unclear. The aim of this systematic review was to assess the association of serum galectin-3 levels with overall survival and cardiovascular outcomes among hemodialysis patients.MethodsMedline, Scopus, Web of Science and CENTRAL were systematically searched from inception till Aug 20, 2023. Observational studies evaluating the association of serum galectin-3 with mortality, cardiovascular disease and arterial stiffness in hemodialysis patients were included. The exposure–response relationship between galectin-3 and mortality was explored by dose–response meta-analysis using restricted cubic splines in a one-stage approach.ResultsOverall, 13 studies were included (9 cohort and 4 cross-sectional), comprising 6025 hemodialysis individuals. Increasing galectin-3 values were associated with greater all-cause mortality risk (χ2: 18.71, p-value < 0.001) and an insignificant trend toward higher cardiovascular mortality risk (χ2: 5.06, p-value: 0.079). Compared to a reference galectin-3 value of 10 ng/ml, all-cause mortality risk was significantly higher with levels of 20 ng/ml (Hazard ratio–HR: 2.62, 95% confidence intervals-CI: 1.66–4.15), 30 ng/ml (HR: 3.78, 95% CI: 2.05–6.97) and 40 ng/ml (HR: 4.01, 95% CI: 2.14–7.52). Qualitative synthesis of evidence indicated that serum galectin-3 may be linked to abdominal aortic calcification severity and progression, as well as to left ventricular systolic and diastolic dysfunction.ConclusionsThis study suggests that high serum galectin-3 levels are associated with greater all-cause mortality risk among patients on maintenance hemodialysis. Preliminary cross-sectional evidence indicates that serum galectin-3 may be associated with arterial stiffness and left ventricular dysfunction.

Exploratory Assessment of Galectin-1, -3, and -9 in Non-Small Cell Lung Cancer.

Galectins play a pivotal role in lung cancer oncogenic pathways, influencing apoptosis, angiogenesis, and tumor metastasis. Biomarkers that diagnose, prognose, and guide cancer treatment are crucial, with galectins having the biomarker potential for non-small cell lung cancer (NSCLC). Using enzyme-linked immunosorbent assay (ELISA), we assessed serum galectin-1, -3, and -9 levels in NSCLC patients. A retrospective chart review was performed to examine patient demographics, cancer stage, tumor biology, cancer treatment, and patient outcomes. Galectin levels were then compared across these factors. In this exploratory analysis, galectin-3 levels were significantly lower in patients with squamous cell lung cancer (p = 0.0019) and in patients exposed to chemotherapy (p = 0.0375). Galectin-1 levels were significantly lower in patients with previous metastasis but had no correlation with future metastasis. Abnormal galectin-1 levels were significantly correlated with decreased overall survival (OS) in NSCLC (p = 0.0357) and specifically in patients with surgically resectable NSCLC (p = 0.0112). However, abnormal galectin-1 levels were not found to correlate with decreased OS in multivariable analysis (p = 0.0513). These findings may have clinical implications as galectin-3 inhibitors are in trials for NSCLC. Additionally, they suggest that galectin-1 has potential as a prognostic marker for surgically resectable NSCLC.

Galectin-3 levels in children with cystic fibrosis.

Cystic fibrosis (CF) is a multisystemic disease in which airway obstruction, infection, and inflammation play a critical role in the pathogenesis and progression of CF lung disease. The carbohydrate-binding protein Galectin-3 is increased in several inflammatory and fibrotic diseases and has recently been forwarded as a biomarker in these diseases. We aimed to define the role of serum Galectin-3 in children with CF by comparison with healthy subjects. This is a cross-sectional, case-control study. 143 CF and 30 healthy subjects were enrolled in the study. Peripheral blood and sputum concentrations of Galectins-3, interleukin (IL)-17A, IL-8, and neutrophil elastase (NE) were determined with commercial ELISA kits. There was no significant difference between the groups in age and gender (p = 0.592, p = 0.613, respectively). Serum Galectin-3 and NE concentrations were higher in the patient group than in healthy controls (p = 0.002, p < 0.001, respectively). There were no significant differences between groups according to IL-17A and IL-8 concentrations. Serum Galectin-3 was correlated with age (r = 0.289, p < 0.001) and body mass index (BMI) (r = 0.493, p < 0.001) in children with CF. Sputum Galectin-3 levels are negatively correlated with percent predictive forced expiratory volume in 1s (FEV1) (r = - 0.297, p = 0.029), FEV1 z-score, (r = - 0.316, p = 0.020), percent predictive forced vital capacity (FVC) (r = - 0.347, p = 0.010), and FVC z-score (r = - 0.373, p = 0.006). Conclusion: The study shows that serum Galectin-3 levels increased in clinically stable CF patients, and serum Galectin-3 response may depend on age, gender, and BMI. The sputum Galectin-3 was found to be negatively correlated with patients' lung functions. What is known: • Galectin-3 is a key regulator of chronic inflammation in the lung, liver, kidney, and tumor microenvironment. What is new: • Children with cystic fibrosis (CF) have higher serum Galectin-3 concentrations than healthy children. • Serum Galectin-3 expression influenced by age, BMI, and gender in children with CF.

Time-course analysis of liver and serum galectin-3 in acute liver injury after alpha-galactosylceramide injection.

Galectin-3 is a beta-galactoside-binding lectin that plays important roles in diverse physiological functions, such as cell proliferation, apoptosis, and mRNA splicing. This protein is expressed on inflammatory cells and acts as a local inflammatory mediator. Recently, galectin-3 has been detected in several diseases, such as chronic liver, heart, and kidney diseases, diabetes, viral infection, autoimmune and neurodegenerative diseases, and tumors, and its role as a biomarker has attracted attention. Alpha-galactosylceramide is an artificially synthesized sphingolipid that can induce acute liver injury via the natural killer T pathway. However, the pathophysiological roles and kinetics of galectin-3 in acute liver injury are not fully understood. This study aimed to elucidate the expression and time course of galectin-3 in liver tissues during acute liver injury following alpha-galactosylceramide injection. Animals were histologically examined on days 1, 2, 4, and 7 after intraperitoneal injection of alpha-galactosylceramide, and the expressions of galectin-3 and ionized calcium-binding adaptor molecule 1 were analyzed. Notably, galectin-3 formed characteristic cluster foci, particularly on day 2 after injection. Cluster formation was not observed in chronic liver disease. Simultaneously, ionized calcium-binding adaptor molecule 1-positive cells were observed in the cluster foci. Serum galectin-3 levels increased on day 2 of treatment and correlated well with the number of galectin-3-positive cell clusters in the liver. Moreover, galectin-3 expression was an important mediator of the early phase of liver injury after alpha-galactosylceramide injection. These results suggest that serum galectin-3 may be a biomarker for the early diagnosis of acute liver injury and that clusters of galectin-3-positive cells may be a specific finding in acute liver injury.

Serum Galectin-1, Galectin-9, and YKL-40 levels in bipolar disorder and their relationship with cognitive functions.

The number of studies conducted on the role of neuroinflammation in the etiopathogenesis of bipolar disorder has been increasing in recent years. The role of Galectin-1, Galectin-9, and YKL-40, which are considered to play roles in neuroinflammation and the etiopathogenesis of bipolar disorder, and the relationship of these parameters with cognitive functions were investigated in the present study. Serum Galectin-1, Galectin-9, and YKL-40 levels were measured with the ELISA Method in 64 bipolar euthymic patients and 64 healthy controls. The Stroop and trail-making tests were administered to assess cognitive functions in all participants. Serum Galectin-1, Galectin-9, and YKL-40 levels were statistically and significantly lower in the patient group when compared to the healthy control group. The scores of the Stroop test and trail-making tests were statistically higher in the patient group than in the healthy control group. There was a weak and positive correlation between serum Galectin-1, Galectin-9, and YKL-40 levels and cognitive performance in all participants. Statistically significant low levels of serum Galectin-1, Galectin-9, and YKL-40 detected in the patient group suggest that these parameters have important roles in neuroinflammation. The statistically higher Stroop and trail-making test scores of the patient group compared to the control group indicates that the cognitive performance of the patient group was weaker. Also, the positive correlation between Galectin-1, Galectin-9, and YKL-40 levels and cognitive performance suggests that these molecules may have a neuroprotective role. We think that the present study will contribute to this field where there is very limited data in the literature.

Associations of galectin-3 levels with measures of vascular disease in patients with rheumatoid arthritis

ObjectivesGalectin-3 is a beta-galactoside-binding lectin and is a marker of cardiovascular disease (CVD) in the general population. It may also play a role in joint inflammation. We asked whether serum galectin-3 is a useful marker of subclinical vascular disease in patients with rheumatoid arthritis (RA). MethodsRA patients without clinical CVD underwent assessment of coronary artery calcium (CAC) score, aortic inflammation (using 18Fluorodeoxyglucose positron emission-computed tomography [FDG PET/CT]), and myocardial flow reserve (MFR). Aorta FDG uptake was measured as standardized uptake values (SUV). Generalized linear models were constructed to explore the associations of galectin-3 levels with CAC score, aortic SUV, and MFR. ResultsA total of 124 RA patients (mean age 57; 82 % women, 45 % Hispanic; median RA duration 6.8 years; 75 % seropositive; median CDAI 16; 33 % on prednisone; 89 % on DMARDs; median CAC score 0; median aorta SUV 2.59; mean MFR 2.86; median galectin-3 level 8.54 ng/mL) were analyzed. In univariable analysis, higher galectin-3 levels were associated with higher aortic SUV (p = 0.007) but CAC score and MFR were not. In multivariable analysis, higher galectin-3 level remained significantly associated with higher aortic SUV (ß Coefficient=0.1786, p value=0.002). ConclusionIn our cohort of RA patients without clinical CVD, higher serum galectin-3 levels were independently associated with higher levels of aortic inflammation, but not CAC score or MFR. This suggests that galectin-3 may be a biomarker for an inflammatory and potentially reversible stage, but not a later (calcified) stage, of atherosclerosis in patients with RA.

Mediating effect of vascular calcification in galectin-3-related mortality in hemodialysis patients

Galectin-3 levels have been studied as a potential biomarker for predicting cardiovascular (CV) risk and mortality in hemodialysis (HD) patients. Recently, a close relationship between galectin-3 and vascular calcification (VC) has been reported. Here, we investigated the role of VC as a mediating factor in the association between galectin-3 and mortality. Serum galectin-3 and baseline aortic arch calcification (AoAC) score were measured in 477 incident HD patients. Mortality data were obtained at a median follow-up of 40 months. Causal mediation analysis was performed to examine the effect of vascular risk factors on galectin-3-related mortality. The prevalence of AoAC in HD patients was 57% (n = 272), and elevated galectin-3 levels were associated with a significantly increased risk of AoAC. When the galectin-3 level was divided by the median level of 37 ng/mL, a higher galectin group increased the risk of all-cause mortality by 1.71-fold (95% CI 1.02–2.92, p = 0.048), even after adjustment for multiple CV risk factors. Mediation analysis showed that both the direct effect of the galectin-3 on mortality (β = 0.0368, bootstrapped 95% CI [0.0113–0.0622]) and the indirect effects were significant. AoAC score and high-sensitivity CRP levels significantly mediated the association between galectin-3 and mortality (total indirect effects: β = 0.0188, bootstrapped 95% CI [0.0066–0.0352]). This study suggests that the association between high galectin-3 and mortality may be partially mediated by higher VC and inflammatory state in HD patients.

Study of Serum Gremlin-1, Galectin-3, and Oxyntomodulin in Women with Breast Cancer

Study of Serum Gremlin-1, Galectin-3, and Oxyntomodulin in Women with Breast Cancer

Diagnostic Value of Serum Galectin-3 Binding Protein Level in Patients with Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) still lacks effective biomarkers to assist in its diagnosis and prognosis. Galectin-3 binding protein (Gal-3BP) plays a role in immune and inflammatory diseases. This study aimed to evaluate Gal-3BP as a prognostic and predictive factor in patients with PAH. From January 2017 to December 2019, we enrolled 167 consecutive PAH patients and 58 healthy controls. Right heart catheterization (RHC) was used to diagnose PAH. Serum Gal-3BP levels were measured by high-sensitivity human enzyme-linked immunosorbent assay (ELISA). Serum Gal-3BP levels in the PAH group were significantly higher compared with the control group (4.87±2.09 vs 2.22±0.86 μg/mL, p<0.001). Gal-3BP level was correlated with several hemodynamic parameters obtained from RHC (p<0.001). Multivariate linear regression analysis showed that Gal-3BP was a risk factor for PAH (odds ratio (OR)=2.947, 95% CI: 1.821-4.767, p<0.001). The optimal cut-off value of serum Gal-3BP level for predicting PAH was 2.89 μg/mL (area under the curve (AUC)=0.860, 95 % CI: 0.811-0.910, p<0.001). Kaplan-Meier analysis showed that Gal-3BP levels above the median (4.87 μg/mL) were associated with an increased risk of death in patients with PAH (hazard ratio (HR)=8.868, 95 % CI: 3.631-21.65, p<0.0001). Cox multivariate risk regression analysis showed that Gal-3BP was a risk factor for death in PAH patients (HR=2.779, 95 % CI: 1.823-4.237, p<0.001). Serum Gal-3BP levels were increased in patients with PAH, and levels of Gal-3BP were associated with the severity of PAH. Gal-3BP might have predictive value for the diagnosis and prognosis of PAH.

Comparison of Preoperative and Postoperative Serum Galectin-3 Levels in Patients Newly Diagnosed with Non-Metastatic Breast Cancer

Comparison of Preoperative and Postoperative Serum Galectin-3 Levels in Patients Newly Diagnosed with Non-Metastatic Breast Cancer

Galectin-3 in Blood Serum and Lymphocytes as a Marker of Myocardial Damage in Patients with Arterial Hypertension and COVID-19.

The constant increase of arterial hypertension and the development of pathology at an earlier age are global healthcare problems that cause damage to vital organs and worsen patient prognosis. In recent years, studies have shown that galectin-3 plays a role in the development and progression of arterial hypertension and coronavirus disease (COVID-19). The explanatory research study aimed to analyze the prognostic value of galectin-3 determination in the serum blood and lymphocytes of patients with arterial hypertension and coronavirus disease (COVID-19). The patients were divided into two groups: Group 1 consisted of 36 individuals with AH, Group 2 included 35 patients with arterial hypertension and polysegmental COVID-19 pneumonia, and 16 practically healthy individuals were included in the control group. All patients underwent anthropometry, biochemical blood analysis, determination of galectin-3, level in serum and lymphocytes, IL-1β, IL-6, and echocardiography. The highest level of galectin-3 was found in patients of Group 1, while in patients of Group 2, the concentration of galectin-3 was significantly decreased, mostly due to the treatment of COVID-19, in addition to prolonged antihypertensive therapy. The level of galectin-3 in serum and lymphocytes was significantly higher in patients of both groups compared to the control group (p<0.05). Arterial hypertension causes structural changes in the cardiovascular system that are associated with elevated levels of galectin-3 in serum and lymphocytes. It can be used as a marker of myocardial damage in the context of arterial hypertension and COVID-19.

Association between serum Galectin-3 and periodontitis in patients with type 2 diabetes mellitus.

This study aims to investigate the correlation between serum Galectin-3 levels and the risk of periodontitis in patients with type 2 diabetes mellitus (T2DM). A total of 140 patients with T2DM admitted to the endocrinology department of Weifang People's Hospital, Affiliated to Weifang Medical College from July 2021 to November 2022 were selected and divided into T2DM without periodontitis group (T2DM group, n=67) and T2DM with periodontitis group (T2DMP group, n=73) according to whether they were combined with periodontitis. In the same period, 65 non-periodontitis volunteers with normal blood glucose were selected as healthy control group (NC group). Blood samples of all subjects were collected, and serum Galectin-3 levels and related laboratory indices were detected and compared among the three groups. Serum Galectin-3 levels in the NC, T2DM, and T2DMP groups were 3.81 (3.49, 4.15), 4.82 (4.25, 5.26), and 6.83 (5.19, 7.28) ng/mL, respectively. After adjusting for the influence of baseline data by multiple linear regression, serum Galectin-3 levels in the T2DMP and T2DM groups were significantly higher than those in the NC group (all P<0.05). Multiple linear regression analysis showed that serum Galectin-3 levels were positively correlated with homeostatic model of the insulin resistance index (β=0.254, 95%CI:0.089-0.419, P=0.003), glycosylated hemoglobin A1c (β=0.397, 95%CI: 0.049-0.745, P=0.026), and clinical attachment loss (β=0.298, 95%CI: 0.024-0.572, P=0.033). After adjusting for the effects of covariates, binary logistic regression showed that serum Galectin-3 levels were significantly associated with the risk of periodontitis in patients with T2DM (OR=2.146, 95%CI: 1.260-3.655, P=0.005). Trend test showed that the risk of periodontitis in patients with T2DM increased with increasing serum Galectin-3 levels (Ptrend=0.011). Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) of serum Galectin-3 in predicting T2DM periodontitis was 0.861 (95%CI: 0.801-0.920, Z=11.806, P<0.001). Serum Galectin-3 levels were elevated in patients with T2DM and pe-riodontitis and associated with the risk of periodontitis.

Prognostic Value of Galectin-3 after Left Atrial Appendage Occlusion for Predicting Peri-Device Leakage

Echocardiographic detection of residual peri-device leakage (PDL) after percutaneous left atrial appendage occlusion (LAAO) is crucial for managing anticoagulation. Galectin-3, a protein involved in tissue–foreign body interactions, may hold significance in understanding PDL and cardiac tissue remodeling after LAAO. This study aimed to analyze galectin-3 serum levels in relation to PDL using a novel echo-morphological classification. LAAO eligible patients were included in the study. Galectin-3 serum levels were measured before LAAO, at 45 days (45D), and at 6 months (6M) after the procedure. Transesophageal echocardiography was used to assess LAAO success. A new echo-morphological classification categorized the degree of LAAO into three different types (A: homogenous echodensity, indicating completely thrombosed device; B: inhomogeneous echolucencies (&lt;50% of device); and C: partially thrombosed device with echolucencies &gt; 50%). Among 47 patients, complete LAAO was achieved in 60% after 45D and in 74% after 6M. We observed a significant increase and distribution of serum levels of galectin-3 [ng/mL] after 45D among the three types (baseline: 13.1 ± 5.8 ng/mL; 45D: 16.3 ± 7.2 ng/mL (Type A) vs. 19.2 ± 8.6 ng/mL (Type B) vs. 25.8 ± 9.4 ng/mL (Type C); p = 0.031), followed by a drop in galectin-3 for Types A and B after 6M toward and below the baseline levels (6M: 8.9 ± 3.1 ng/mL (Type A) vs. 12.4 ± 5.5 ng/mL (Type B)), whereas Type C persisted in showing elevated galectin-3 levels compared to all other types (6M: 17.5 ± 4.5 ng/mL (Type C); p &lt; 0.01). Increased galectin-3 serum levels after LAAO likely reflect the transition from thrombus formation to fibrotic scar development in the LAA lumen. Successful occlusion is associated with a time-restricted decrease in galectin-3 levels after 6 months, while relevant PDL leads to persistently elevated levels, making galectin-3 a potential predictor of occlusion success.

FEATURES OF THE MORPHO-FUNCTIONAL MYOCARDIUM STATE AND RELATIONSHIP WITH GALECTIN-3 IN PATIENTS WITH CHRONIC HEART FAILURE OF ISCHEMIC ORIGIN ON THE BACKGROUND OF METABOLIC PATHOLOGY

The aim. To evaluate the presence and nature of changes in the morpho-functional state of the myocardium in patients with coronary heart disease (CHD) with concomitant type 2 diabetes mellitus (T2DM) and obesity, depending on the functional class (FC) of chronic heart failure (CHF) and the relationship with the concentration of galectin-3 in blood serum.&#x0D; Materials and methods. The study involved 75 patients with CHD with concomitant metabolic diseases such as T2DM and obesity, who were treated in the cardiology department of the State Clinical Hospital No. 27. Patients were divided into groups according to the FC of CHF. Group 1 included 30 patients with CHF FC II, group 2 – 24 patients with CHF FC III, group 3 – 21 patients with CHF FC IV.&#x0D; Results. In patients with СHD and metabolic disorders with CHF FC III, the levels of end-systolic dimension (ESD) and end-diastolic dimension (EDD) were higher by 16.3 % and 17.9 %, respectively, compared with FC II, end-systolic volume (ESV) and end-diastolic volume (EDV) also increased significantly in patients of this cohort with FC III compared with CHF FC II by 35.8 % and 16.5 %, respectively. Significantly increased ESV, EDV by 42.9 % and 37.8 %, respectively, as well as the size of the left atrium by 14.3 % in patients of the study group who had CHF FC IV compared with FC III. The ejection fraction (EF) index decreased in patients of this cohort with CHF FC IV by 14.4 % compared with FC III. The size of the right ventricle was larger by 10.8 % in CHF FC IV than in FC III in patients with CHD on the background of comorbid metabolic pathology. Indicators of the thickness of the LV posterior wall, LV relative wall thickness and intraventricular septum were lower in patients with FC IV compared with FC II, left ventricle mass (LVM) and left ventricle mass index (LVMI) increased by 32 % and 33 %, respectively. Сomparing the levels of Ea/Es in patients with CHF FC II and IV in СHD with concomitant T2DM and obesity, a significant increase in this indicator was found in FC IV (p&lt;0.05). The level of galectin-3 in patients with CHF FC III and IV of ischemic origin against the background of concomitant metabolic disorders was higher than in patients with FC II. Сomparing the concentration of galectin-3 in patients with CHF FC III and IV in patients with CHD with comorbid metabolic pathology, significantly higher levels were found in FC IV (p&lt;0.05). The study of the relationship between the fibrosis factor galectin-3 and cardiohemodynamic parameters revealed probable links, namely direct links between galectinemia and ESV (r=0.52; p&lt;0.05), EDV (r=0.58; p&lt;0.05), Еа/Es (r=0.51; p&lt;0.05).&#x0D; Conclusions. The growth of the functional class of chronic heart failure is accompanied by dilatation of the left cavities of the heart, a decrease in the inotropic function of the left ventricle, an increase in myocardial-arterial stiffness, and an increase in the levels of the galectin-3 fibrosis factor in the studied patients.

Abstract 16799: Galectin-1 Alleviates Aortic Valve Calcification via Modulating Integrin-Mediated Cytoskeletal Reorganization and Focal Adhesion

Background Galectin-1, a beta-glycoside binding protein, has been reported to involve a variety of cell functions including proliferation, cell migration and focal adhesion. The role of cell-matrix interaction in calcific aortic valve disease (CAVD) is not fully investigated and whether galectin-1 is involved in this process remains unclear. We hypothesized that galectin-1 mitigates the fibrocalcific response and mechanosensitivity of valve interstitial cells (AVICs) by modulating integrin-mediated cytoskeletal reorganization and focal adhesion. Methods and Results We enrolled patients with CAVD and age- and sex-matched controls to detect serum galectin-1 and found that circulating galectin-1 was lower in CAVD. The expression of galectin-1 decreased in fibrocalcific valves and AVICs cultured in osteogenic medium (OM), as shown by western blot, qPCR, immunohistochemistry (IHC) and immunofluorescence. Silencing galectin-1 by short-interfering RNA exacerbated the fibrocalcific change of AVICs in vitro while recombinant galectin-1 (rGal-1) prevented these effects. AVICs cultured in OM also presented enhanced integrin signaling, cytoskeletal reorganization and focal adhesion. Anti-integrin blocking experiments and co-immunoprecipitation assays demonstrated that the galectin-1 directly interacted with integrin αvβ1 to regulate AVICs adhesion to a fibronectin matrix. Western blot, qPCR and Immunofluorescence assays confirmed that actin cytoskeletal reorganization was induced by αvβ1 activation through Rac1-WRC-Arp2/3 signaling axis. Western blot, alkaline phosphatase (ALP) as well as Alizarin red staining demonstrated that silencing galectin-1 enhanced AVICs sensitivity to piezo1 activation, which is dependent on αvβ1 binding and actin polymerization. In vivo, aortic valve disease was constructed by direct wire injury (DWI), and we showed that overexpression of galectin-1 by adeno-associated virus significantly decelerated the progression of aortic valve lesion induced by DWI in mice. Conclusion Galectin-1 interacts with integrin αvβ1 to modulate cytoskeletal reorganization and AVICs adhesion to fibronectin, thus mitigating the fibrocalcific response of AVICs and aortic valve calcification.

Serum Galectin-3: A novel predictor of treatment response to cryotherapy in cutaneous warts

Serum Galectin-3: A novel predictor of treatment response to cryotherapy in cutaneous warts

Galectin-3 as a Biomarker to Predict Cardiorenal Syndrome in Patients with Acute Heart Failure.

Galectin-3 affects cardiac tissue inflammation as an inflammatory mediator. The development of cardiorenal syndrome in heart failure patients is associated with a poor prognosis. This study aims to investigate whether serum galectin-3 levels can be used as a biomarker to predict cardiorenal syndrome in heart failure patients with reduced left ventricular ejection fraction. A total of 166 symptomatic heart failure patients [New York Heart Association (NYHA) functional class II-III] with reduced left ventricular ejection fraction (≤ 40%) were recruited prospectively. Cardiorenal syndrome type 1 was defined as an acute worsening of cardiac function leading to renal dysfunction. The patients were divided into two groups with and without cardiorenal syndrome. The galectin-3 levels of all patients were determined. The primary outcome of this study was the occurrence of cardiorenal syndrome. Cardiorenal syndrome developed in 41 patients. Galectin-3 levels were found to be higher in the patients with cardiorenal syndrome (+) compared to those without cardiorenal syndrome (-) (20.7 ± 2.9 ng/mL vs. 17.8 ± 3.1 ng/mL, p < 0.001). After performing a multivariable analysis, galectin-3 levels [odds ratio (OR): 3.21, p = 0.001], NYHA functional class (OR: 1.98, p = 0.009), creatinine (OR: 3.18, p = 0.006), furosemide dose (OR: 1.21, p = 0.033), and angiotensin-converting enzyme inhibitor/angiotensin-receptor blockers usage (OR: 0.54, p = 0.029) were identified as independent predictors for the development of cardiorenal syndrome. Moreover, galectin-3 level demonstrated predictive capability for cardiorenal syndrome development (AUC = 0.761, p < 0.001). Serum galectin-3 level showed an association with cardiorenal syndrome development in patients with heart failure, indicating potential usefulness as a prognostic biomarker.

Increased Levels of Galectin-3 in Critical COVID-19.

Severe COVID-19 is related to hyperinflammation and multiple organ injury, including respiratory failure, thus requiring intensive care unit (ICU) admission. Galectin-3, a carbohydrate-binding protein exhibiting pleiotropic effects, has been previously recognized to participate in inflammation, the immune response to infections and fibrosis. The aim of this study was to evaluate the relationship between galectin-3 and the clinical severity of COVID-19, as well as assess the prognostic accuracy of galectin-3 for the probability of ICU mortality. The study included 235 COVID-19 patients with active disease, treated in two different Greek hospitals in total. Our results showed that median galectin-3 serum levels on admission were significantly increased in critical COVID-19 patients (7.2 ng/mL), as compared to the median levels of patients with less severe disease (2.9 ng/mL, p = 0.003). Galectin-3 levels of the non-survivors hospitalized in the ICU were significantly higher than those of the survivors (median 9.1 ng/mL versus 5.8 ng/mL, p = 0.001). The prognostic accuracy of galectin-3 for the probability of ICU mortality was studied with a receiver operating characteristic (ROC) curve and a multivariate analysis further demonstrated that galectin-3 concentration at hospital admission could be assumed as an independent risk factor associated with ICU mortality. Our results were validated with galectin-3 measurements in a second patient cohort from a different Greek university hospital. Our results, apart from strongly confirming and advancing previous knowledge with two patient cohorts, explore the possibility of predicting ICU mortality, which could provide useful information to clinicians. Therefore, galectin-3 seems to establish its involvement in the prognosis of hospitalized COVID-19 patients, suggesting that it could serve as a promising biomarker in critical COVID-19.