scholarly journals GALECTIN-3: A NOVEL BIOMARKER FOR THE PROGNOSIS OF HEART FAILURE

2017 ◽  
Vol 90 (2) ◽  
pp. 129-132 ◽  
Author(s):  
Hilman Zulkifli Amin ◽  
Lukman Zulkifli Amin ◽  
Ika Prasetya Wijaya
Keyword(s):  
Heart Failure ◽  
Cardiac Fibrosis ◽  
Ventricular Remodeling ◽  
Prognostic Biomarker ◽  
Global Burden ◽  
Prediction Tool ◽  
Galectin 3 ◽  
Substantial Risk ◽  
Loading And Unloading ◽  
Food And Drugs Administration

Heart failure (HF) is still a global burden which carries substantial risk of morbidity and mortality. Thus, appropriate approach of diagnosis and layering the prognosis of HF are of great importance. In this paper we discuss and review a novel biomarker, which is called galectin-3 and already approved by Food and Drugs Administration (FDA) as a prediction tool for HF.Galectin-3, which is secreted by macrophages under the influence of mediators like osteopontin, has been known for its significant role in mediating cardiac fibrosis and inflammation. Numerous studies have shown galectin-3 as a novel prognostic biomarker with high predictive value for cardiovascular mortality and re-hospitalization in HF patients. However, there are also other contradictive studies displayed galectin-3 inferiority against other existed HF prognostic biomarkers like NT-proBNP and ST2. Nevertheless, galectin-3 has some advantages such as more stability and resistance against hemodynamic loading and unloading state, and also it could act as an early indicator of cardiac fibrosis, ventricular remodeling, and renal impairment in HF patients.

scholarly journals GALECTIN-3, MMP-9 AND ST-2: BIOCHEMICAL MARKERS IN CARDIOVASCULAR DISEASES

2018 ◽  
Vol 24 (3) ◽  
pp. 281
Author(s):  
Anak Agung Wiradewi Lestari
Keyword(s):  
Heart Failure ◽  
Cardiac Fibrosis ◽  
Ventricular Remodeling ◽  
Panel Member ◽  
Post Discharge ◽  
Pharmacological Agents ◽  
Galectin 3 ◽  
Coronary Syndromes ◽  
And Function

Galectin-3 is a reasonably stable biomarker. It can be detected even before the onset of heart failure occurs. Heart Failure (HF) is one of the complications of AMI as well as one of the major cardiovascular parameters. One study showed that elevated levels of Galectin-3 that persisted up to 3-6 months of the follow-up period in patients with heart failure were associated with a poorer prognosis. Many studies explain that the role of Galectin-3 is strong in cardiac remodeling/fibrosis and the occurrence of heart failure. Inhibition of Galectin-3 by pharmacological agents has been shown to be able to the prevent that cardiac fibrosis process, particularly in patients with advanced heart failure. Since its discovery as a gene product induced by cardiomyocyte stretch in vitro, ST2 has emerged as a powerful player with IL-33 in modulating ventricular function and remodeling via effects on apoptosis, inflammation and myocardial fibrosis. Clinically, measurement of sST2 appears promising as a biomarker for remodeling and outcome across the AHA HF Stages. Circulating levels of sST2 are strongly related to short and long-term post-discharge mortality in acute coronary syndromes and HF, as well as markers of cardiac structure and function. Current pre-clinical and clinical documentation strongly support MMP-9 as a panel member in the biomarker list to diagnose or treat the pathophysiology of post-MI ventricular remodeling and congestive heart failure. Based on the evidence provided, further prospective studies are required to assess the prognostic value of MMP-9 for post-MI remodeling, particularly in comparison with traditional markers.  

scholarly journals GALECTIN-3, MMP-9 AND ST-2: BIOCHEMICAL MARKERS IN CARDIOVASCULAR DISEASES

2018 ◽  
Vol 24 (3) ◽  
pp. 281
Author(s):  
Anak Agung Wiradewi Lestari
Keyword(s):  
Heart Failure ◽  
Cardiac Fibrosis ◽  
Ventricular Remodeling ◽  
Panel Member ◽  
Post Discharge ◽  
Pharmacological Agents ◽  
Galectin 3 ◽  
Coronary Syndromes ◽  
And Function

Galectin-3 is a reasonably stable biomarker. It can be detected even before the onset of heart failure occurs. Heart Failure (HF) is one of the complications of AMI as well as one of the major cardiovascular parameters. One study showed that elevated levels of Galectin-3 that persisted up to 3-6 months of the follow-up period in patients with heart failure were associated with a poorer prognosis. Many studies explain that the role of Galectin-3 is strong in cardiac remodeling/fibrosis and the occurrence of heart failure. Inhibition of Galectin-3 by pharmacological agents has been shown to be able to the prevent that cardiac fibrosis process, particularly in patients with advanced heart failure. Since its discovery as a gene product induced by cardiomyocyte stretch in vitro, ST2 has emerged as a powerful player with IL-33 in modulating ventricular function and remodeling via effects on apoptosis, inflammation and myocardial fibrosis. Clinically, measurement of sST2 appears promising as a biomarker for remodeling and outcome across the AHA HF Stages. Circulating levels of sST2 are strongly related to short and long-term post-discharge mortality in acute coronary syndromes and HF, as well as markers of cardiac structure and function. Current pre-clinical and clinical documentation strongly support MMP-9 as a panel member in the biomarker list to diagnose or treat the pathophysiology of post-MI ventricular remodeling and congestive heart failure. Based on the evidence provided, further prospective studies are required to assess the prognostic value of MMP-9 for post-MI remodeling, particularly in comparison with traditional markers.  

Galectin-3 in Heart Failure – Linking Fibrosis, Remodelling and Progression

2010 ◽  
Vol 6 (2) ◽  
pp. 33 ◽  
Author(s):  
Christopher R deFilippi ◽  
G Michael Felker ◽  
◽  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Risk Stratification ◽  
Cardiac Fibrosis ◽  
The Elderly ◽  
Preserved Ejection Fraction ◽  
Heart Failure Patients ◽  
Large Populations ◽  
Galectin 3

For many with heart failure, including the elderly and those with a preserved ejection fraction, both risk stratification and treatment are challenging. For these large populations and others there is increasing recognition of the role of cardiac fibrosis in the pathophysiology of heart failure. Galectin-3 is a novel biomarker of fibrosis and cardiac remodelling that represents an intriguing link between inflammation and fibrosis. In this article we review the biology of galectin-3, recent clinical research and its application in the management of heart failure patients.

scholarly journals Short- and Long-term Biologic Variability of Galectin-3 and Other Cardiac Biomarkers in Patients with Stable Heart Failure and Healthy Adults

2016 ◽  
Vol 62 (2) ◽  
pp. 360-366 ◽  
Author(s):  
Emily I Schindler ◽  
Jeffrey J Szymanski ◽  
Karl G Hock ◽  
Edward M Geltman ◽  
Mitchell G Scott
Keyword(s):  
Heart Failure ◽  
Troponin I ◽  
Prognostic Biomarker ◽  
High Sensitivity ◽  
Cardiac Biomarkers ◽  
Healthy Individuals ◽  
Short Term ◽  
Galectin 3 ◽  
Short And Long Term

Abstract BACKGROUND Galectin-3 (Gal-3) has been suggested as a prognostic biomarker in heart failure (HF) patients that may better reflect disease progression than traditional markers, including B-type natriuretic peptide (BNP) and cardiac troponins. To fully establish the utility of any biomarker in HF, its biologic variability must be characterized. METHODS To assess biologic variability, 59 patients were prospectively recruited, including 23 male and 16 female patients with stable HF and 10 male and 10 female healthy individuals. Gal-3, BNP, and high-sensitivity cardiac troponin I (hs-cTnI) were assayed at 5 time points within a 3-week period to assess short-term biologic variability. Long-term (3-month) biologic variability was assessed with samples collected at enrollment and after 4, 8, and 12 weeks. RESULTS Among healthy individuals, mean short-term biologic variability, expressed as intraindividual CV (CVI), was 4.5% for Gal-3, 29.0% for BNP, and 14.5% for hs-cTnI; long-term biologic variability was 5.5% for Gal-3, 34.7% for BNP, and 14.7% for hs-cTnI. In stable HF patients, mean short-term biologic variability was 7.1% for Gal-3, 22.5% for BNP, and 8.5% for hs-cTnI, and mean long-term biologic variability was 7.7% for Gal-3, 27.6% for BNP, and 9.6% for hs-cTnI. CONCLUSIONS The finding that Gal-3 has minimal intraindividual biological variability adds to its potential as a useful biomarker in HF patients.

Amperometric galectin-3 immunosensor-based gold nanoparticle-functionalized graphitic carbon nitride nanosheets and core–shell Ti-MOF@COFs composites

Nanoscale ◽  
2020 ◽  
Vol 12 (38) ◽  
pp. 19824-19832 ◽  
Author(s):  
Mehmet Lütfi Yola ◽  
Necip Atar
Keyword(s):  
Heart Failure ◽  
Gold Nanoparticle ◽  
Carbon Nitride ◽  
Cardiac Fibrosis ◽  
Graphitic Carbon Nitride ◽  
Core Shell ◽  
Death Risk ◽  
Failure Risk ◽  
Galectin 3 ◽  
Carbon Nitride Nanosheets

Antigen galectin-3 (GL-3), a member of β-galactoside proteins indicates cardiac fibrosis and is a significant biomarker for monitoring heart failure risk and death risk.

scholarly journals Protein kinase C promotes cardiac fibrosis and heart failure by modulating galectin-3 expression

2015 ◽  
Vol 1853 (2) ◽  
pp. 513-521 ◽  
Author(s):  
Xiang Song ◽  
Xiaoqian Qian ◽  
Ming Shen ◽  
Rong Jiang ◽  
Mary B. Wagner ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cardiac Fibrosis ◽  
Kinase C ◽  
Galectin 3

scholarly journals Galectin-3 in Predicting Mortality of Heart Failure: A Systematic Review and Meta-Analysis

2021 ◽  
Vol 24 (2) ◽  
pp. E327-E332
Author(s):  
Chenxia Wu ◽  
Zhengtian Lv ◽  
Xinyi Li ◽  
Xinbing Zhou ◽  
Wei Mao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Systematic Review ◽  
Chronic Heart Failure ◽  
Cardiac Fibrosis ◽  
Inflammatory Marker ◽  
Meta Analysis ◽  
Cochrane Library ◽  
Heart Failure Patients ◽  
Galectin 3 ◽  
The Cochrane Library

Background: In recent years, galectin-3, an inflammatory marker, has been demonstrated to be closely related to cardiac fibrosis and heart failure. The purpose of this systematic review and meta-analysis is to define galectin-3 in predicting mortality of heart failure. Methods: PubMed, Embase, and the Cochrane Library were searched. A total of 1540 studies were identified, and of these studies, 19 involving 9217 patients were included in our meta-analysis. Results: The diagnostic hazard ratios of galectin-3 in predicting mortality in chronic heart failure patients was 1.13 (95% CI,:1.07-1.21 ) and 2.17 (95% CI:1.27-3.08) in acute heart failure (HF) patients. Conclusions: Our meta-analysis shows that elevated levels of galectin-3 are associated with higher mortality in both acute and chronic heart failure patients.

scholarly journals Galectin-3 and the Development of Heart Failure after Acute Coronary Syndrome: Pilot Experience from PROVE IT-TIMI 22

2012 ◽  
Vol 58 (1) ◽  
pp. 267-273 ◽  
Author(s):  
E Wilson Grandin ◽  
Petr Jarolim ◽  
Sabina A Murphy ◽  
Lea Ritterova ◽  
Christopher P Cannon ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Coronary Syndrome ◽  
Cardiac Fibrosis ◽  
Coronary Syndrome ◽  
Patients With Heart Failure ◽  
Galectin 3 ◽  
Adverse Remodeling ◽  
Nested Case Control ◽  
The Relationship ◽  
Control Study

Abstract BACKGROUND Galectin-3 is a β-galactoside–binding lectin that has been implicated in cardiac fibrosis and remodeling, is increased in models of failure-prone hearts, and has prognostic value in patients with heart failure (HF). The relationship between galectin-3 and the development of HF after acute coronary syndrome (ACS) is unknown. METHODS In a nested case-control study among patients with ACS in PROVE IT-TIMI 22, we identified 100 cases with a hospitalization for new or worsening HF. Controls were matched (1:1) for age, sex, ACS type, and randomized treatment. Serum galectin-3 was measured at baseline (within 7 days post-ACS). RESULTS Patients who developed HF had higher baseline galectin-3 [median 16.7 μg/L (25th, 75th percentile 14.0, 20.6) vs 14.6 μg/L (12.0, 17.6), P = 0.004]. Patients with baseline galectin-3 above the median had an odds ratio of 2.1 (95% CI 1.2–3.6) for developing HF, P = 0.010. Galectin-3 showed a graded relationship with risk of HF. Cases were more likely to have hypertension, diabetes, prior MI, and prior HF; after adjustment for these factors, this graded relationship with galectin-3 quartile and HF remained significant [adjusted OR 1.4 (95% CI 1.1–1.9), P = 0.020]. When BNP was added to the model, the relationship between galectin-3 and HF was attenuated [adjusted OR 1.3 (95% CI: 0.96–1.9), P = 0.08]. CONCLUSIONS The finding that galectin-3 is associated with the risk of developing HF following ACS adds to emerging evidence supporting galectin-3 as a biomarker of adverse remodeling contributing to HF as well as a potential therapeutic target.

scholarly journals Galectin-3 in Cardiovascular Diseases

2020 ◽  
Vol 21 (23) ◽  
pp. 9232
Author(s):  
Valeria Blanda ◽  
Umberto Marcello Bracale ◽  
Maria Donata Di Taranto ◽  
Giuliana Fortunato
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Cardiac Fibrosis ◽  
Cellular Adhesion ◽  
Cellular Growth ◽  
Cardiac Inflammation ◽  
Galectin 3 ◽  
Diagnostic Applications

Galectin-3 (Gal-3) is a β-galactoside-binding protein belonging to the lectin family with pleiotropic regulatory activities and several physiological cellular functions, such as cellular growth, proliferation, apoptosis, differentiation, cellular adhesion, and tissue repair. Inflammation, tissue fibrosis and angiogenesis are the main processes in which Gal-3 is involved. It is implicated in the pathogenesis of several diseases, including organ fibrosis, chronic inflammation, cancer, atherosclerosis and other cardiovascular diseases (CVDs). This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodelling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis.

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