The role of galectin-3 in heart failure and cardiovascular disease

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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

European Cardiology Review ◽

10.15420/ecr.2010.6.2.33 ◽

2010 ◽

Vol 6 (2) ◽

pp. 33 ◽

Cited By ~ 10

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.

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Biomarkers for the diagnosis and management of heart failure

Heart Failure Reviews ◽

10.1007/s10741-021-10105-w ◽

2021 ◽

Author(s):

Vincenzo Castiglione ◽

Alberto Aimo ◽

Giuseppe Vergaro ◽

Luigi Saccaro ◽

Claudio Passino ◽

...

Keyword(s):

Heart Failure ◽

Risk Stratification ◽

Adverse Outcome ◽

Volume Overload ◽

High Sensitivity ◽

Circulating Biomarkers ◽

Diagnosis And Management ◽

Conflicting Evidence ◽

Galectin 3

AbstractHeart failure (HF) is a significant cause of morbidity and mortality worldwide. Circulating biomarkers reflecting pathophysiological pathways involved in HF development and progression may assist clinicians in early diagnosis and management of HF patients. Natriuretic peptides (NPs) are cardioprotective hormones released by cardiomyocytes in response to pressure or volume overload. The roles of B-type NP (BNP) and N-terminal pro-B-type NP (NT-proBNP) for diagnosis and risk stratification in HF have been extensively demonstrated, and these biomarkers are emerging tools for population screening and as guides to the start of treatment in subclinical HF. On the contrary, conflicting evidence exists on the role of NPs as a guide to HF therapy. Among the other biomarkers, high-sensitivity troponins and soluble suppression of tumorigenesis-2 are the most promising biomarkers for risk stratification, with independent value to NPs. Other biomarkers evaluated as predictors of adverse outcome are galectin-3, growth differentiation factor 15, mid-regional pro-adrenomedullin, and makers of renal dysfunction. Multi-marker scores and genomic, transcriptomic, proteomic, and metabolomic analyses could further refine HF management.

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Abstract 14: Cardiac Biomarkers are Associated With Findings on Brain MRI in Older Adults: The Atherosclerosis Risk in Communities (ARIC) Study

Circulation ◽

10.1161/circ.141.suppl_1.14 ◽

2020 ◽

Vol 141 (Suppl_1) ◽

Cited By ~ 1

Author(s):

Andreea M Rawlings ◽

Christie M Ballantyne ◽

Rebecca F Gottesman ◽

Ron C Hoogeveen ◽

Timothy M Hughes ◽

...

Keyword(s):

Heart Failure ◽

Atrial Fibrillation ◽

Cardiovascular Disease ◽

Coronary Heart Disease ◽

Heart Disease ◽

Troponin T ◽

Brain Mri ◽

Standard Deviation Increase ◽

Cortical Volume ◽

Galectin 3

Background: Cerebrovascular disease is often the consequence of cardiac disease. Our aim was to examine associations of biomarkers of cardiovascular disease, high sensitivity troponin T (hs-cTnT), NT-proBNP, and galectin-3, with cerebrovascular signs: lacunar infarcts, lobar and subcortical microhemorrhages, cortical infarcts, and white matter hyperintensity (WMH) volume. We also examined total cortical and Alzheimer’s Disease (AD) signature region volumes. Methods: We conducted a cross-sectional analysis of 1748 ARIC participants from the 2011-2013 exam who had biomarker measurements, completed a brain MRI, and did not have a clinical history of stroke. We used linear regression to model brain volumes, modeled as Z scores, and logistic regression for all other outcomes; biomarkers were log transformed. We repeated analyses excluding persons with coronary heart disease, atrial fibrillation, and heart failure. Results: The mean age of participants was 76, 62% were female, and 21% were Black. All biomarkers were associated with total cortical volume. Each standard deviation increase in log hs-cTnT was associated with lower total cortical volume (adjusted beta = -0.08, 95% CI: -0.12, -0.05); results for the other biomarkers were similar (Figure). All biomarkers were associated with lobar microhemorrhages. Hs-cTnT and NT-proBNP were associated with WMH volume, but galectin-3 was not. No biomarker was associated with subcortical microhemorrhages or cortical infarcts. Results were similar in persons without coronary heart disease, atrial fibrillation, or heart failure (conditions associated with cerebral thromboembolism). Conclusions: In persons free of clinical cardiovascular disease, biomarkers of cardiac stretch, strain, and fibrosis were associated cerebral small vessel disease and reduced cortical volume, but not in a specific pattern suggestive of AD pathogenesis. This suggests subclinical vascular insults affect brain structure through mixed pathogenic processes.

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The Evolving Role of Angiotensin Receptor Blockers in Heart Failure

Hospital Pharmacy ◽

10.1177/001857870203700505 ◽

2002 ◽

Vol 37 (5) ◽

pp. 474-482

Author(s):

Patricia A. Howard

Keyword(s):

Heart Failure ◽

Cardiovascular Disease ◽

Angiotensin Receptor Blockers ◽

Angiotensin Receptor ◽

Cardiovascular Pharmacotherapy ◽

The Us ◽

Prevention And Treatment ◽

Recent Developments ◽

Receptor Blockers

This continuing feature will update readers on recent developments in cardiovascular pharmacotherapy. Cardiovascular disease remains the number one killer in the US, and more clinical outcome trials have been conducted in cardiology than in any other field of medicine. Given this rapidly expanding knowledge base, pharmacists can have a significant impact on the prevention and treatment of cardiovascular disease—if they keep current with developments in drug therapy.

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Intestinales Mikrobiom und kardiovaskuläre Erkrankungen

DMW - Deutsche Medizinische Wochenschrift ◽

10.1055/a-0746-4002 ◽

2019 ◽

Vol 144 (14) ◽

pp. 957-963

Author(s):

Hans-Michael Steffen ◽

Münevver Demir

Keyword(s):

Physical Activity ◽

Risk Factors ◽

Heart Failure ◽

Blood Pressure ◽

Cardiovascular Disease ◽

Vascular Function ◽

Kardiovaskuläre Erkrankungen ◽

Intestinal Microbiome ◽

Current Review

AbstractAging, physical activity, bodyweight and diet are well established risk factors for cardiovascular disease. For all of these factors a great impact on the intestinal microbiome has been described. The current review will discuss available data regarding the role of the gut microbiome in regulating blood pressure, vascular function and its possible contribution to atherosclerosis and heart failure.

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Dysfunction of the β2-spectrin-based pathway in human heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00875.2015 ◽

2016 ◽

Vol 310 (11) ◽

pp. H1583-H1591 ◽

Cited By ~ 15

Author(s):

Sakima A. Smith ◽

Langston D. Hughes ◽

Crystal F. Kline ◽

Amber N. Kempton ◽

Lisa E. Dorn ◽

...

Keyword(s):

Heart Failure ◽

Cardiovascular Disease ◽

Left Ventricle ◽

Small Animal ◽

Left Ventricular ◽

Effector Proteins ◽

Human Heart Failure ◽

Protein Levels ◽

Ankyrin B

β2-Spectrin is critical for integrating membrane and cytoskeletal domains in excitable and nonexcitable cells. The role of β2-spectrin for vertebrate function is illustrated by dysfunction of β2-spectrin-based pathways in disease. Recently, defects in β2-spectrin association with protein partner ankyrin-B were identified in congenital forms of human arrhythmia. However, the role of β2-spectrin in common forms of acquired heart failure and arrhythmia is unknown. We report that β2-spectrin protein levels are significantly altered in human cardiovascular disease as well as in large and small animal cardiovascular disease models. Specifically, β2-spectrin levels were decreased in atrial samples of patients with atrial fibrillation compared with tissue from patients in sinus rhythm. Furthermore, compared with left ventricular samples from nonfailing hearts, β2-spectrin levels were significantly decreased in left ventricle of ischemic- and nonischemic heart failure patients. Left ventricle samples of canine and murine heart failure models confirm reduced β2-spectrin protein levels. Mechanistically, we identify that β2-spectrin levels are tightly regulated by posttranslational mechanisms, namely Ca2+- and calpain-dependent proteases. Furthermore, consistent with this data, we observed Ca2+- and calpain-dependent loss of β2-spectrin downstream effector proteins, including ankyrin-B in heart. In summary, our findings illustrate that β2-spectrin and downstream molecules are regulated in multiple forms of cardiovascular disease via Ca2+- and calpain-dependent proteolysis.

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Role of the fatty acid-binding protein 4 in heart failure and cardiovascular disease

Journal of Endocrinology ◽

10.1530/joe-17-0031 ◽

2017 ◽

Vol 233 (3) ◽

pp. R173-R184 ◽

Cited By ~ 39

Author(s):

Ricardo Rodríguez-Calvo ◽

Josefa Girona ◽

Josep M Alegret ◽

Alba Bosquet ◽

Daiana Ibarretxe ◽

...

Keyword(s):

Heart Failure ◽

Cardiovascular Disease ◽

Fatty Acid ◽

Fatty Acid Binding Protein ◽

Binding Protein ◽

Left Ventricular ◽

Aetiological Factor ◽

Fatty Acid Binding ◽

Acid Binding Protein

Obesity and ectopic fat accumulation in non-adipose tissues are major contributors to heart failure (HF) and cardiovascular disease (CVD). Adipocytes act as endocrine organs by releasing a large number of bioactive molecules into the bloodstream, which participate in a communication network between white adipose tissue and other organs, including the heart. Among these molecules, fatty acid-binding protein 4 (FABP4) has recently been shown to increase cardiometabolic risk. Both clinical and experimental evidence have identified FABP4 as a relevant player in atherosclerosis and coronary artery disease, and it has been directly related to cardiac alterations such as left ventricular hypertrophy (LVH) and both systolic and diastolic cardiac dysfunction. The available interventional studies preclude the establishment of a direct causal role of this molecule in CVD and HF and propose FABP4 as a biomarker rather than as an aetiological factor. However, several experimental reports have suggested that FABP4 may act as a direct contributor to cardiac metabolism and physiopathology, and the pharmacological targeting of FABP4 may restore some of the metabolic alterations that are conducive to CVD and HF. Here, we review the current knowledge regarding FABP4 in the context of HF and CVD as well as the molecular basis by which this protein participates in the regulation of cardiac function.

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Role of galectin-3 and plasma B type-natriuretic peptide in predicting prognosis in discharged chronic heart failure patients

Medicine ◽

10.1097/md.0000000000004014 ◽

2016 ◽

Vol 95 (26) ◽

pp. e4014 ◽

Cited By ~ 10

Author(s):

Mauro Feola ◽

Marzia Testa ◽

Laura Leto ◽

Marco Cardone ◽

Mario Sola ◽

...

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Natriuretic Peptide ◽

Heart Failure Patients ◽

Galectin 3

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Follistatin-like 1 in Cardiovascular Disease and Inflammation

Mini-Reviews in Medicinal Chemistry ◽

10.2174/1389557519666190312161551 ◽

2019 ◽

Vol 19 (16) ◽

pp. 1379-1389 ◽

Cited By ~ 3

Author(s):

Marijn M.C. Peters ◽

Timion A. Meijs ◽

Wouter Gathier ◽

Pieter A.M. Doevendans ◽

Joost P.G. Sluijter ◽

...

Keyword(s):

Heart Failure ◽

Cardiovascular Disease ◽

Posttranslational Modifications ◽

Cardiac Regeneration ◽

Regenerative Therapy ◽

Coronary Syndrome ◽

Disease Mechanisms ◽

Spatiotemporal Regulation ◽

Shed Light

: Follistatin-like 1 (FSTL1), a secreted glycoprotein, has been shown to participate in regulating developmental processes and to be involved in states of disease and injury. Spatiotemporal regulation and posttranslational modifications contribute to its specific functions and make it an intriguing candidate to study disease mechanisms and potentially develop new therapies. With cardiovascular diseases as the primary cause of death worldwide, clarification of mechanisms underlying cardiac regeneration and revascularization remains essential. Recent findings on FSTL1 in both acute coronary syndrome and heart failure emphasize its potential as a target for cardiac regenerative therapy. With this review, we aim to shed light on the role of FSTL1 specifically in cardiovascular disease and inflammation.

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