Galectin-3: A Novel Biomarker for the Prognosis of Heart Failure

Amin, Hilman Zulkifli; Amin, Lukman Zulkifli; Wijaya, Ika Prasetya

doi:10.15386/cjmed-751

Cited by 38 publications

(40 citation statements)

References 27 publications

(49 reference statements)

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“…Although various biomarkers are reported for accessing prognosis of heart failure patients, most of them remained inconclusive. In the present investigation, gal‐3 showed a noteworthy promising result (AUC: 0.70, P < .0001) for diagnosis of heart failure compared to other galectins which is in line with earlier reports . Furthermore, when we analyse role of galectin in sever heart failure cases, gal‐3 emerged as a potent molecular marker of severe clinical manifestation (AUC: 0.82, P < .0001).…”

Section: Discussionsupporting

confidence: 91%

Galectin‐3 is associated with severe heart failure and death: A hospital‐based study in Chinese patients

Wang¹,

Dang²,

Zhang³

et al. 2020

Scand J Immunol

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Heart failure (HF) is a serious disease syndrome characterized by elevated proinflammatory cytokines and inflammatory mediators presume to have significant contribution on disease progression. Galectins are carbohydrate-binding proteins responsible of various physiological functions. Role of galectins in heart failure has been ill-defined. In the present case-controls study, 136 patients clinically diagnosed with heart failure and 125 healthy Chinese controls were recruited. Levels of galec-

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Section: Discussionsupporting

confidence: 91%

Galectin‐3 is associated with severe heart failure and death: A hospital‐based study in Chinese patients

Wang¹,

Dang²,

Zhang³

et al. 2020

Scand J Immunol

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“…Galectin-3 (Gal-3) affects the pathogenesis of many diseases, including heart failure and arteriosclerosis [6][7]. It belongs to a family of β-galactoside-binding lectins and plays an important role in cellular physiological and pathological processes, such as cell proliferation, adhesion, differentiation, angiogenesis, inflammation and fibrosis, all of which are important for the development of vessel remodeling and stiffness.…”

Section: Introductionmentioning

confidence: 99%

Galectin-3- Mediated Transdifferentiation of Pulmonary Artery Endothelial Cells Contributes to Hypoxic Pulmonary Vascular Remodeling

Zhang

Zeng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Vascular muscularity is a key event in vessel remodeling during pulmonary artery hypertension (PAH). Endothelial-mesenchymal transdifferentiation (EndMT) has been increasingly reported to play a role in disease occurrence. Galectin-3, a carbohydrate-binding protein regulates cell proliferation, differentiation, migration and neovascularization. However, whether galectin-3 controls endothelial cell transdifferentiation during the development of PAH is unknown. Methods: Rats were exposed to normoxic or hypoxic conditions (fraction of inspired O₂ 0.10) for 21 d to establish PAH models. Hemodynamic changes were evaluated through surgery of the right jugular vein and ultrasound biomicroscopy inviVue. And vessel pathological alterations were detected by H&E staining. Galectin-3 (Gal-3)-induced pulmonary artery endothelium cell (PAEC) dynamic alterations were measured by MTT assays, Cell immunofluorescence, Flow cytometry, Real-time PCR and Western blot. Results: Our study demonstrated that Gal-3 was expressed in hypoxic pulmonary vascular adventitia and intima. The increased Gal-3 expression was responsible for hypoxic vessel remodeling and PAH development in vivo. Gal-3 was found to inhibit cell proliferation and apoptosis in cultured endothelial cells. Meanwhile endothelial cell morphology was altered and exhibited smooth muscle-like cell features as demonstrated by the expression of α-SMA after Gal-3 treatment. Gal-3 activated Jagged1/Notch1 pathways and induced MyoD and SRF. When MyoD or SRF were silenced with siRNAs, Gal-3-initiated transdifferentiation in endothelial cells was blocked as indicated by a lack of α-SMA. Conclusion: These results suggest that Gal-3 induces PAECs to acquire an α-SMA phenotype via a transdifferentiation process which depends on the activation of Jagged1/Notch1 pathways that mediate MyoD and SRF expression.

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“…Galectin‐3 is involved in numerous physiological and pathological processes, including fibrosis and inflammation, which are critical contributing pathophysiological mechanisms to the development and progression of HF . Elevated Galectin‐3 stimulates the release of various mediators and promotes cardiac fibroblast proliferation and ventricular dysfunction .…”

Section: Discussionmentioning

confidence: 99%

“…18,19,50 Galectin-3 is involved in numerous physiological and pathological processes, including fibrosis and inflammation, which are critical contributing pathophysiological mechanisms to the development and progression of HF. 10,[20][21][22] Elevated Galectin-3 stimulates the release of various mediators and promotes cardiac fibroblast proliferation and ventricular dysfunction. 23 Both ST2 and Galectin-3 were included in the American Heart Association guidelines as additive risk stratification biomarkers for acute and chronic HF in adults.…”

Section: Discussionmentioning

confidence: 99%

Biomarkers associated with 30‐day readmission and mortality after pediatric congenital heart surgery

et al. 2019

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Objectives Novel cardiac biomarkers serum (suppression of tumorigenicity [ST2]) and Galectin‐3 may be associated with an increased likelihood of important events after cardiac surgery. Our objective was to explore the association between pre‐ and postoperative serum biomarker levels and 30‐day readmission or mortality for pediatric patients. Methods We prospectively enrolled pediatric patients <18 years of age who underwent at least one cardiac surgical operation at Johns Hopkins Children's Center from 2010 to 2014 (N = 162). Blood samples were collected immediately before surgery and at the end of bypass. We evaluated the association between pre‐ and postoperative Galectin‐3 and ST2 with 30‐day readmission or mortality, using backward stepwise logistic regression, adjusting for covariates based on the Society of Thoracic Surgeons (STS) Congenital Heart Surgery Mortality Risk Model. Results In our cohort, 21 (12.9%) patients experienced readmission or mortality 30‐days from discharge. Before adjustment, preoperative ST2 terciles demonstrated a strong association with readmission and/or mortality after surgery (OR: 2.58; 95% CI: 1.17‐3.66 and OR: 4.37; 95% CI: 1.31‐14.57). After adjustment for covariates based on the STS congenital risk model, Galectin‐3 postoperative mid‐tercile was significantly associated with 30‐day readmission or mortality (OR: 6.17; 95% CI: 1.50‐0.43) as was the highest tercile of postoperative ST2 (OR: 4.98; 95% CI: 1.06‐23.32). Conclusions Elevated pre‐and postoperative levels of ST2 and Galectin‐3 are associated with increased risk of readmission or mortality after pediatric heart surgery. These clinically available biomarkers can be used for improved risk stratification and may guide improved patient care management.

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Galectin-3: A Novel Biomarker for the Prognosis of Heart Failure

Cited by 38 publications

References 27 publications

Galectin‐3 is associated with severe heart failure and death: A hospital‐based study in Chinese patients

Galectin‐3 is associated with severe heart failure and death: A hospital‐based study in Chinese patients

Galectin-3- Mediated Transdifferentiation of Pulmonary Artery Endothelial Cells Contributes to Hypoxic Pulmonary Vascular Remodeling

Biomarkers associated with 30‐day readmission and mortality after pediatric congenital heart surgery

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