The Association of Serum Galectin‐3 Levels with Atrial Electrical and Structural Remodeling

Yalçın, Muhammed Ulvi; Gürses, Kadri Murat; Koçyiğit, Duygu; Canpınar, Hande; Canpolat, Uğur; Evranos, Banu; Yorgun, Hikmet; Şahiner, Mehmet Levent; Kaya, Ergün Barış; Hazırolan, Tuncay; Tokgözoğlu, Lâle; Oto, Mehmet Ali; Özer, Necla; Güç, Dicle; Aytemir, Kudret

doi:10.1111/jce.12637

Cited by 67 publications

(67 citation statements)

References 37 publications

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“…Our data showed that PeAF patients had higher levels of circulating Gal-3 than SR control patients. This is in agreement with another study showing that persistent atrial fibrillation was an independent predictor of higher Gal-3 concentrations [11], and Gal-3 levels were found to be higher in patients with persistent atrial fibrillation and in those with cardiovascular risk factors [35]. With respect to sampling site differences, circulating Gal-3 in AF patients possibly originates not only from the heart but could also reflect systemic fibrosis and inflammation levels, and as reported previously, Gal-3 levels are higher peripherally than in intra-cardiac samples from patients undergoing catheter ablation for atrial fibrillation [30].…”

Section: Discussionsupporting

confidence: 82%

Activation of TGF-β1/α-SMA/Col I Profibrotic Pathway in Fibroblasts by Galectin-3 Contributes to Atrial Fibrosis in Experimental Models and Patients

Shen

Wang

Min

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study aimed to evaluate whether galectin-3 (Gal-3) contributes actively to atrial fibrosis both in patients and experimental atrial fibrillation (AF) models. Methods: Mouse HL-1 cardiomyocytes were subjected to rapid electrical stimulation (RES) to explore Gal-3 expression and secretion levels by western blotting (WB) and enzyme linked immunosorbent assay (ELISA). Neonatal rat cardiac fibroblasts were treated with conditioned culture medium and recombinant human Gal-3 to evaluate the activation of the transforming growth factor (TGF)-β1/α-smooth muscle actin (SMA)/collagen I (Col I) profibrotic pathway (WB) and fibroblast proliferation with a Cell Counting Kit-8 (CCK-8). Furthermore, in the rapid atrial pacing (RAP) rabbit AF model, atrial Gal-3 expression and its effects on the profibrotic pathway were evaluated (WB and Masson’s trichrome staining). Moreover, 44 consecutive patients who underwent single mitral valve repair/replacement were included, consisting of 28 patients with persistent AF (PeAF) and 16 with sinus rhythm (SR). Coronary sinus blood was also sampled to test circulating Gal-3 levels (ELISA), and atrial myocardium Gal-3 and its downstream TGF-β1/α-SMA pathway were also measured by WB and immunohistochemical staining. Results: Gal-3 expression in HL-1 cells and its secretion level in culture medium were greatly increased after 24 h RES. Treatment of neonatal rat cardiac fibroblasts with conditioned media collected from the RES group or recombinant human Gal-3 protein (10 and 30 µg/mL) for 72 h induced the activation of the TGF-β1/α-SMA/Col I profibrotic pathway. RAP increased Gal-3 levels and activated the TGF-β1/α-SMA/Col I pathway in rabbit left atria, while the Gal-3 inhibitor N-acetyllactosamine, injected at 4.5 mg/kg every 3 days, mitigated these adverse changes. Furthermore, Gal-3 levels in coronary sinus blood samples and myocardial Gal-3 expression levels were higher in the PeAF patients than in the SR patients, and higher level profibrotic pathway activation was also confirmed. Conclusions: Activation of Gal-3 expression in the atria can subsequently activate the TGF-β1/α-SMA/Col I pathway in cardiac fibroblasts, which may enhance atrial fibrosis.

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Section: Discussionsupporting

confidence: 82%

Activation of TGF-β1/α-SMA/Col I Profibrotic Pathway in Fibroblasts by Galectin-3 Contributes to Atrial Fibrosis in Experimental Models and Patients

Shen

Wang

Min

et al. 2018

Cell Physiol Biochem

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“…Recently, Yalcin et al performed a nested-case control study including patients with paroxysmal AF who underwent delayed-enhancement magnetic resonance imaging prior to cryoballoon-based AF ablation. A significant correlation was found between serum levels of galectin-3 and extent of left atrium fibrotic burden [24]. The results of the present study showed that galectin-3 levels increased somewhat in paroxysmal AF patients.…”

Section: Discussionsupporting

confidence: 63%

Galectin-3: A biochemical marker to detect paroxysmal atrial fibrillation?

Selçoki¹,

Aydın²,

Çelik³

et al. 2016

CIM

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Purpose: Atrial fibrillation (AF) is the most common form of arrhythmia. AF leads to electrical remodelling and fibrosis of the atria; however, the mechanism(s) remain poorly understood. Galectin-3 is a potential mediator of cardiac fibrosis. The present study aimed to examine the relationship between serum galectin-3 levels and paroxysmal AF.Methods: Forty-six patients with paroxysmal AF and preserved left ventricular systolic function, and 38 age-and gender-matched control subjects, were involved in the study. Serum galectin-3 levels were analyzed with an enzyme-linked immunosorbent assay (ELISA).Results: Serum galectin-3 levels (median 1.38 ng/mL; 1.21 ng/mL-1.87 ng/mL; p< 0.001) were significantly elevated in patients with paroxysmal AF compared with the control. Left atrial diameter was significantly higher in patients with paroxysmal AF (41.2±3.0 mm vs. 39.6±3.3 mm). Left atrial diameter was found to be significantly correlated with serum galectin-3 levels in patients with paroxysmal AF (r= 0.378, p= 0.001).Conclusion: Serum galectin-3 levels are significantly elevated and significantly correlated with left atrial diameter in patients with paroxysmal AF.SUPPLEMENT

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“…In addition, a combination of established biomarkers elevated during HF and associated with atrial remodelling might contribute to the development of risk scores: e.g. BNP54 and Galectin‐3120 have been shown to be markers of atrial remodelling and to directly correlate with the extent of LA fibrosis 121. Only recently has TNF‐alpha been suggested as a biomarker for increased fibrosis, cardiomyocyte apoptosis, and AF 122.…”

Section: Discussionmentioning

confidence: 99%

Atrial remodelling in heart failure: recent developments and relevance for heart failure with preserved ejection fraction

et al. 2018

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The Association of Serum Galectin‐3 Levels with Atrial Electrical and Structural Remodeling

Abstract: This is a hypothesis-generating study pointing out that serum galectin-3 level is significantly associated with atrial remodeling in paroxysmal AF patients with preserved LV function. Further studies are necessary to provide exact pathophysiological mechanisms.

Cited by 67 publications

References 37 publications

Activation of TGF-β1/α-SMA/Col I Profibrotic Pathway in Fibroblasts by Galectin-3 Contributes to Atrial Fibrosis in Experimental Models and Patients

Activation of TGF-β1/α-SMA/Col I Profibrotic Pathway in Fibroblasts by Galectin-3 Contributes to Atrial Fibrosis in Experimental Models and Patients

Galectin-3: A biochemical marker to detect paroxysmal atrial fibrillation?

Atrial remodelling in heart failure: recent developments and relevance for heart failure with preserved ejection fraction

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