The serum MANF in patients with AF was markedly lower than that in patients with SR, which was inversely correlated with atrial apoptosis in patients with AF.
MPO levels were significantly increased in AF patients compared to controls (median, 27.7 ng/ml (IQR 14.3-66.6) versus 12.6 (IQR 9.9-17.7), p < 0.001), without differences between clinical AF progression phenotypes.
The aim of the present study was to determine whether CYP2J2/EET has a preventive effect on atrial fibrillation (AF) and to investigate the underlying mechanisms.
Moreover, our findings are consistent with the hypothesis that TRPC3 channel up-regulation leads to abnormal accumulation of collagen, with the down-regulation of SIRT1 as an aetiological factor of high Hcy, which in turn predisposes to atrial fibrosis and strongly enhances the possibility of AF.
The comparison of the patient cohorts in the AFA and AFG registries showed that AF ablation in European clinical practice is mostly performed in relatively young, symptomatic and relatively healthy patients.
We investigated whether growth differentiation factor-15 (GDF-15), also known as macrophage inhibitory cytokine-1 (MIC-1), levels are associated with a prothrombotic state in atrial fibrillation (AF) as compared to N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin I (cTnI-hs).
The competing endogenous RNA (ceRNA) network analysis revealed two upregulated genes, IFNG and GDF7, and one downregulated gene, BMP7, all of which were involved in TGF-beta signaling pathway, which further suggested that these circRNAs, namely hsa_circ_0000075 and hsa_circ_0082096, participated in the AF pathogenesis via TGF-beta signaling pathway.
LA pump strain and GLS were significantly and independently associated with AF and provided incremental predictive value over clinical and standard echocardiographic parameters.
The competing endogenous RNA (ceRNA) network analysis revealed two upregulated genes, IFNG and GDF7, and one downregulated gene, BMP7, all of which were involved in TGF-beta signaling pathway, which further suggested that these circRNAs, namely hsa_circ_0000075 and hsa_circ_0082096, participated in the AF pathogenesis via TGF-beta signaling pathway.
Here, we investigated the effect of ubiquitin C-terminal hydrolase 1 (UCHL1), an important DUB, on the development of AF induced by angiotensin II (Ang II).
Here, we investigated the effect of ubiquitin C-terminal hydrolase 1 (UCHL1), an important DUB, on the development of AF induced by angiotensin II (Ang II).
This analysis from the EMPA-REG OUTCOME trial explores CV and renal outcomes in patients with vs. without AF at baseline and assesses the benefits of empagliflozin.
Here, we investigated the effect of ubiquitin C-terminal hydrolase 1 (UCHL1), an important DUB, on the development of AF induced by angiotensin II (Ang II).
IGF-1 levels and IGF-1/IGFBP-3 ratios were significantly lower in individuals with AF than in those without AF (IGF-1: 104.2 ± 41.6 ng/mL vs 142.9 ± 53.5 ng/mL, P < .001 and IGF-1/IGFBP-3: 0.031 ± (0.009 ng/mL vs 0.036 ± 0.010 ng/mL, P = .006, respectively).
All these eight lncRNAs that were identified from previous steps (RP11-363E7.4, GAS5, RP11-410L14.2, HAGLR, RP11-421L21.3, RP11-111K18.2, HOTAIRM1, and RP11-296O14.3) exhibited a strong diagnostic power for AF.
According to the multiple logistic regression model, age and levels of UA, direct bilirubin (DBIL), and gamma-glutamyl transpeptidase (GGT) were important risk factors for predicting AF.
Patients with AF had significantly lower MFR than patients without [MFR: 1.87; 95% confidence interval (CI) 1.58-2.22 vs. 2.50; 95% CI 2.06-2.86; percent difference: -21.5%; P = 0.01].
Our results provide a new evidence that miR-27b-3p regulates the signaling pathway of Wnt/<i>β</i>-Catenin by targeting Wnt3a, which may play an important role in the development of atrial fibrosis and AF.