Galectin-3 in Patients with Atrial Fibrillation Undergoing Radiofrequency Catheter Ablation

Kornej, Jelena; Schmidl, Josephin; Ueberham, Laura; John, Silke; Daneschnejad, Sait S; Dinov, Borislav; Hindricks, Gerhard; Adams, Volker; Husser, Daniela; Bollmann, Andreas

doi:10.1371/journal.pone.0123574

Cited by 49 publications

(52 citation statements)

References 23 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: 93%

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: 93%

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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“…Among the 38 full‐text articles assessed for eligibility, ten were excluded for the following reasons: One study lacked a control group; one study population was heart failure; four studies lacked available data for further analysis; and four reported duplicate data from studies that later published as full text . Finally, 28 studies involving 10 830 patients were included in our meta‐analysis, with their baseline characteristics shown in Tables and .…”

Section: Resultsmentioning

confidence: 99%

Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

Gong

Cheung

Wang

et al. 2020

Clinical Laboratory Analysis

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Background Galectin‐3 is an inflammatory marker that is raised in myocardial fibrosis and inflammation. Recent studies have explored its role in predicting atrial fibrillation (AF) outcomes. The aim of this systematic review and meta‐analysis is to examine the association between serum concentration of galectin‐3 and AF. Methods PubMed, EMBASE, and the Cochrane Database were searched. A total of 280 studies were identified, of which 28 studies involving 10 830 patients were included in our meta‐analysis. Results Galectin‐3 is present at higher concentrations in patients with AF than those in sinus rhythm (mean difference [MD] = −0.68 ng/mL, 95% CI: −0.92, −0.44, Z = 5.61, P < .00001). Galectin‐3 levels were significantly higher in the persistent AF than in the paroxysmal AF group (MD = −0.94 ng/mL, 95% CI: −1.85, −0.03, Z = 2.04, P = .04). Higher galectin‐3 levels were associated with a 45% increase in the odds of developing AF (odds ratio [OR] = 1.45, 95% CI: 1.15, 1.83, Z = 3.11, P = .002) and risk of AF recurrence (hazard ratio [HR] =1.17, 95% CI: 1.06, 1.29, Z = 3.12, P = .002). Conclusions Our meta‐analysis found that galectin‐3 is significantly higher in patients with persistent AF than in those with paroxysmal AF, and can predict both AF development and recurrence after treatment.

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“…8 Galectin-3 has been associated with atrial remodeling in AF patients 9 and outcomes after catheter ablation of atrial AF. 10,11 Recent epidemiologic studies have shown that blood levels of galectin-3 are associated positively with incident heart failure (HF) and coronary heart disease (CHD), 6,12–14 but to our knowledge, only 2 prospective studies of exclusively whites have tested whether galectin-3 concentrations are associated with incident AF. Both studies reported positive associations that were no longer significant after adjusting for traditional AF risk factors.…”

mentioning

confidence: 99%

Galectin-3 and incidence of atrial fibrillation: The Atherosclerosis Risk in Communities (ARIC) study

Fashanu

Norby

Aguilar

et al. 2017

American Heart Journal

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Background Galectin-3, a beta-galactoside binding lectin involved in important regulatory roles in adhesion, inflammation, immunity, and fibrosis, may be relevant to atrial fibrillation (AF) etiology. Methods We included 8,436 participants free of AF at baseline (1996–98) and with measures of plasma galectin-3 from the Atherosclerosis Risk in Communities (ARIC) study. We ascertained incident AF through 2013 from study visit ECGs, hospitalizations and death certificates. Multivariable Cox proportional hazards models, adjusted for AF risk factors plus incident HF and CHD, were used to estimate hazard ratios for the association between galectin-3 and incident AF. Results The mean age (SD) of participants was 62.6 (5.6) years and was comprised of 58.7% women and 21.2% blacks. During a median follow-up of 15.7 years, 1,185 incident cases of AF were observed. After adjusting for AF risk factors, participants with galectin-3 levels ≥ 90th percentile (19.5 ng/mL) had a significantly higher risk of incident AF when compared to the lowest quartile (4.4 – 11.9 ng/mL), with hazard ratios (95% confidence interval) of 1.40 (1.04 – 1.89) for the 90th – <95th percentile and 1.51 (1.11 – 2.06) for the 95th – 100th percentile. This association was attenuated and no longer statistically significant after accounting for incident CHD and HF as time dependent variables. Conclusions Elevated plasma galectin-3 is associated with increased risk of incident AF. Galectin-3 may increase AF risk via pathways involving CHD and HF.

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Galectin-3 in Patients with Atrial Fibrillation Undergoing Radiofrequency Catheter Ablation

Cited by 49 publications

References 23 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 and risk of atrial fibrillation: A systematic review and meta‐analysis

Galectin-3 and incidence of atrial fibrillation: The Atherosclerosis Risk in Communities (ARIC) study

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