RESUMEN
BACKGROUND: As the burden of mental disorders among patients with atrial fibrillation (AF) increases, researchers are beginning to pay close attention to the risk and prevalence of these comorbidities. Although studies have independently analyzed the risk of comorbidity with depression and anxiety in patients with AF, no study has systematically focused on the global epidemiology of these two mental disorders. AIM: To explore the prevalence of depression and anxiety in patients with AF. METHODS: Five databases were searched from their date of establishment until January 2023. Observational studies reporting the comorbidity of AF with depression and anxiety, were included in this study. Basic information, such as the first author/ publication year, study year, study type, and prevalence of depression and anxiety, were extracted. STATA SE 15.1 was used to analyze the data. Subgroup, meta-regression, and sensitivity analyses were performed to estimate study heterogeneity. RESULTS: After a thorough search, 26 studies were identified and included in this meta-analysis. The prevalence rates of depression and anxiety in adults with AF were 24.3% and 14.5%, respectively. Among adult males with AF, the prevalence was 11.7% and 8.7%, respectively, whereas in females it was 19.8% and 10.1%, respectively. In older adults with AF, the prevalence rates of depression and anxiety were 40.3% and 33.6%, respectively. The highest regional prevalence of depression and anxiety was observed in European (30.2%) and North American (19.8%) patients with AF. CONCLUSION: In this study, we found that the prevalence of depression and anxiety among patients with AF varies with sex, region, and evaluation scales, suggesting the need for psychological interventions for patients with AF in clinical practice.
RESUMEN
BACKGROUND: Epigallocatechin gallate (EGCG) has multiple biological effects such as anti-tumor multiple drug resistance, antioxidation and anti-inflammatory properties. Ferroptosis is the main driving factor of ischemic heart injury, thus inhibiting ferroptosis may prove to be an effective treatment strategy for cardiovascular diseases. However, the role of EGCG on ferroptosis in ischemic myocardium and underlying mechanisms remain uncertain. PURPOSE: This study was aimed to investigate the effects and potential mechanisms of EGCG on myocardial ischemic-induced ferroptosis both in vitro and in vivo. METHODS: Cardiomyocyte hypoxia model and mouse acute myocardial infarction (AMI) model were established in vitro and in vivo. MiR-450b-5p and ACSL4 silencing or overexpression plasmids were transfected, with or without EGCG pretreatment. Cell viability was determined by the CCK-8 assay. Hematoxylin and eosin (HE) staining and transmission electron microscopy (TEM) were used to evaluate the morphologic alterations. TTC staining was used to observe the infarction area, and echocardiography was adopted to appraise the heart function. Using flow cytometry, the presence of reactive oxygen species (ROS) was assessed. The content of cardiac troponin I (cTn I), glutathione (GSH), malondialdehyde (MDA), divalent iron ions (Fe2+) and superoxide dismutase (SOD) were detected using reagent kits. A luciferase activity assay was performed to assess the binding ability of miR-450b-5p to ACSL4. Expressions of related genes and proteins were measured by RT-qPCR and western blotting respectively. RESULTS: EGCG attenuated AMI-induced ferroptosis and improved myocardial ischemia injury, which was associated with reducing iron deposition and cTn I, inhibition of lipid peroxidation, decreasing TFR1 and ACSL4, and upregulating SLC7A11, FTH1 and GPX4. Meanwhile, EGCG pretreatment increased miR-450b-5p expression in ischemic myocardium. Further researches discovered that knockdown of miR-450b-5p partially compromised EGCG-generated protective effect in hypoxia HL-1 cells, while combination with miR-450b-5p mimic could strengthen the potency of EGCG on ischemic myocardium. The dual-luciferase test demonstrated that miR-450b-5p has binding to ACSL4. Furthermore, silencing of ACSL4 synergistically increased the cardioprotective effect of EGCG. More significantly, EGCG treatment regulated the ferroptosis-related proteins expression via miR-450b-5p/ACSL4 axis. CONCLUSION: In summary, the present study evidently demonstrated that EGCG attenuates myocardial ischemia injury by targeting ferroptosis. Our work revealed the role of miR-450b-5p/ACSL4 axis in AMI for the first time. Further, it also elucidated the molecular mechanisms of EGCG on inhibiting ferroptosis greatly depend on the miR-450b-5p/ACSL4 axis, suggesting that EGCG may act as a novel anti-ferroptosis agent and exert a therapeutic role in AMI.