BACKGROUND Triglyceride-glucose (TyG) index values are a new surrogate marker for insulin resistance. This study aimed to explore the relationship between cumulative TyG index values and atrial fibrillation (AF) recurrence after radiofrequency catheter ablation (RFCA). METHODS A total of 576 patients with AF who underwent RFCA at the Second Affiliated Hospital of Xi’an Jiaotong University were included in this study. The participants were grouped based on cumulative TyG index values tertiles within 3 months after ablation. Cox regression and restricted cubic spline analyses were used to determine the relationship between cumulative TyG index values and AF recurrence. The predictive value of all risk factors was assessed by receiver operating curve analysis. RESULTS There were 375 patients completed the study (age: 63.23 ± 10.73 years, 64.27% male). The risk of AF recurrence increased with increasing cumulative TyG index values tertiles. After adjusting for potential confounders, patients in the medium cumulative TyG index group [hazard ratio (HR) = 4.949, 95% CI: 1.778–13.778, P = 0.002] and the high cumulative TyG index group (HR = 8.716, 95% CI: 3.371–22.536, P < 0.001) had a higher risk of AF recurrence than those in the low cumulative TyG index group. The restricted cubic spline regression model also showed an increased risk of AF recurrence with increasing cumulative TyG index values. When considering cumulative TyG index values, left atrial diameter, and lactate dehydrogenase levels as a comprehensive factor, the model could effectively predict AF recurrence after RFCA [area under the curve (AUC) = 0.847, 95% CI: 0.797–0.897, P < 0.001]. CONCLUSIONS Cumulative TyG index values were a risk factor for AF recurrence after RFCA. Monitoring longitudinal TyG index values may assist with optimized for risk stratification and outcome prediction for AF recurrence.

The present study was focused on whether ABCG1 deficiency was involved in endothelial apoptosis and its possible mechanism. Human umbilical artery endothelial cells were transfected with ABCG1 siRNA and/or ABCG1 expression plasmid. We observed that silencing of endothelial ABCG1 reduced cholesterol efflux to HDL and increased intracellular lipid content. Moreover, reduction of ABCG1 promoted endothelial apoptosis and expression of endoplasmic reticulum (ER) stress-related molecules GRP78 and CHOP. In contrast, transfection of ABCG1 overexpression plasmid reversed endothelial apoptosis and intracellular lipid accumulation as well as decreased expression of GRP78 and CHOP in ABCG1-deficient endothelial cells. Furthermore, endothelial apoptosis and ER stress-related molecules were induced by repletion of endothelial cells with cholesterol-loaded cyclodextrin, otherwise endothelial apoptotic response and expression of GRP78 and CHOP were suppressed by depletion of cellular cholesterol in ABCG1-deficient endothelial cells. The present results suggest that reduction of ABCG1 induces endothelial apoptosis, which seems associated with intracellular free cholesterol accumulation and subsequent ER stress.

Summary. Oxidative stress is an important factor that is related to endothelial dysfunction. ATP-binding cassette transporter G1 (ABCG1), a regulator of intracellular cholesterol efflux, has been found to prevent endothelial activation in vessel walls. To explore the role of ABCG1 in oxidative stress production in endothelial cells, HUAECs were exposed to H₂O₂ and transfected with the specific ABCG1 siRNA or ABCG1 overexpression plasmid. The results showed that overexpression of ABCG1 by ABCG1 plasmid or liver X receptor (LXR) agonist T0901317 treatment inhibited ROS production and MDA content induced by H₂O₂ in HUAECs. Furthermore, ABCG1 upregulation blunted the activity of prooxidant NADPH oxidase and the expression of Nox4, one of the NADPH oxidase subunits. Moreover, the increased migration of Nrf2 from the cytoplasm to the nucleus and antioxidant HO-1 expression were detected in HUAECs with upregulation of ABCG1. Conversely, ABCG1 downregulation by ABCG1 siRNA increased NADPH oxidase activity and Nox4 expression and abrogated the increase at Nrf2 nuclear protein levels. In addition, intracellular cholesterol load interfered with the balance between NADPH oxidase activity and HO-1 expression. It was suggested that ABCG1 attenuated oxidative stress induced by H₂O₂ in endothelial cells, which might be involved in the balance between decreased NADPH oxidase activity and increased Nrf2/OH-1 antioxidant defense signaling via its regulation for intracellular cholesterol accumulation.

Aim: Frailty is an important risk factor for a wide range of chronic diseases and for mortality risk. This study aims to explore the relationship between frailty and incidence of chronic kidney disease (CKD), particularly on the change and accumulation of frailty. Methods: Frailty status was assessed using the frailty index (FI, constructed by 31 items) and categorized as robust, pre-frail, and frail. The accumulation and change in frailty were assessed on the basis of frailty status at baseline and a second survey 4 years after baseline. Logistic regression was used to estimate the association between frailty and developing CKD. Results: A total of 3597 participants (mean age: 59.08 ± 8.94 years old, male: 49.9%) from CHARLS were included. Participants with pre-frailty or frailty status had a higher risk of developing CKD compared with robust participants (pre-frail vs robust, OR 1.78, 95% CI 1.37–2.32, p < 0.001; frail vs robust, OR 2.52, 95% CI 1.67–3.79, p < 0.001). Participants who had a robust status in the two surveys had a significantly lower risk of developing CKD (OR 0.51, 95% CI 0.36–0.75, p < 0.001) compared with those who never had a robust status. Conclusion: Frailty status is significantly associated with the incidence of CKD. The risk of CKD was lower in those who ever had a robust status than in participants who never had a robust status.