Background: The control of diseases related to atrial fibrillation (AF) may reduce the occurrence of AF, delay progression, and reduce complications, which is beneficial to the prevention and treatment of AF. An increasing number of studies have shown that AF is associated with depression. However, to date, there has not been a bibliometric analysis to examine this field systematically. Our study aimed to visualize the publications to determine the hotspots and frontiers in research on AF and depression and provide guidance and reference for further study. Methods: Publications about AF and depression between 2001 and 2021 were retrieved from the Web of Science Core Collection (WOSCC) database. CiteSpace 5.8. R1, VOSviewer 1.6.16, and Excel 2019 software tools were used to conduct this bibliometric study. Results: In total, 159 articles and reviews were analyzed. The number of publications has been increased sharply since 2018. David D. McManus had the largest number of publications. The most prolific country was the USA with 54 publications but the centrality was <0.1. The most prolific institution was Northeastern University. Three clusters were formed based on keywords: The first cluster was composed of atrial fibrillation, depression, anxiety, symptoms, ablation, and quality of life, et al. The second cluster were risk, prevalence, mortality, heart failure, association, et al. While the third cluster included anticoagulation, impact, stroke, management, warfarin, et al. After 2019, stroke and prediction are the keywords with strongest citation bursts. Conclusion: Research on AF and depression is in its infancy. Cooperation and exchanges between countries and institutions must be strengthened in the future. The effect of depression on prevalence and mortality in AF, depression on ablation in AF, and impact of depression on anticoagulation treatment in AF have been the focus of current research. Stroke prevention (including anticoagulant therapy) is the research frontier, which may still be the focus of research in the future.

Platelet-derived exosomes (PLT-Exos) are the main subtype of extracellular vesicles secreted by platelets, which carry proteins, nucleotides, lipids, and other substances to acceptor cells, playing an important role in intercellular communication. PLT-Exos increase with platelet activation and are involved in the process of atherothrombosis by delivering cargo to acceptor cells. Atherosclerotic plaque rupture, causing thrombosis and arterial occlusion, is the basic pathological change leading to cardiovascular events. PLT-Exos from different donors have different functions. PLT-Exos secreted by healthy volunteer or mice can inhibit platelet activation and inflammation of endothelial cells, thus exerting an antithrombotic effect, while PLT-Exos derived from some patients induce endothelial apoptosis and an inflammatory response to promote atherothrombosis. Furthermore, increased PLT-Exos reflect platelet activation and their cargoes also are derived from platelets; therefore, PLT-Exos can also be used as a biomarkers for the diagnosis and prognosis of cardiovascular disease. This article reviews the characteristics of PLT-Exos and discusses their role in cell-to-cell communication and atherothrombosis.

Atrial fibrillation (AF) is a common clinical arrhythmia whose pathogenesis has not been fully elucidated, and the inflammatory response plays an important role in the development of AF. The inflammasome is an important component of innate immunity and is involved in a variety of pathophysiologic processes. The NLRP3 inflammasome is by far the best studied and validated inflammasome that recognizes multiple pathogens through pattern recognition receptors of innate immunity and mediates inflammatory responses through activation of Caspase-1. Several studies have shown that NLRP3 inflammasome activation contributes to the onset and development of AF. Ecological dysregulation of the gut microbiota has been associated with the development of AF, and some evidence suggests that gut microbiota components, functional byproducts, or metabolites may induce or exacerbate the development of AF by directly or indirectly modulating the NLRP3 inflammasome. In this review, we report on the interconnection of NLRP3 inflammasomes and gut microbiota and whether this association is related to the onset and persistence of AF. We discuss the potential value of pharmacological and dietary induction in the management of AF in the context of the association between the NLRP3 inflammasome and gut microbiota. It is hoped that this review will lead to new therapeutic targets for the future management of AF.

The coronary microembolization contributes to coronary microvascular dysfunction (CMD), in which miR-34a-5p may play a critical role. Ligustrazine has been reported to improve CMD. The present study was designed to discuss the role of miR-34a-5p/Sirt1 pathway in CMD and explore the underlying mechanism of ligustrazine. Coronary microembolization (CME) was induced by left ventricle injection of sodium laurate in rats. CME formation and cardiac function were examined by HE staining and hemodynamic tests to evaluate CMD. The expressions of miR-34a-5p, Sirt1 and the downstream proteins were detected by RT-qPCR and western blot. Dual-luciferase reporter (DLR) assay was performed to confirm the connection between miR-34a-5p and Sirt1. The blood markers of endothelial dysfunction, platelet activation and inflammation were examined with ELISA. Overt CME and cardiac dysfunction as well as up-regulated miR-34a-5p and down-regulated Sirt1 were observed in CME rats. Overexpressing miR-34a-5p aggravated while silencing miR-34a-5p inhibited CME formation. DLR assay confirmed that miR-34a-5p directly inhibited Sirt1 mRNA expression. Ligustrazine pretreatment suppressed miR-34a-5p and promoted Sirt1 expression, which alleviated endothelial dysfunction, inhibited platelet activation and inflammation, and in turn reduced CME. Overexpressing miR-34a-5p diminished the positive effects of ligustrazine; while after silencing miR-34a-5p, ligustrazine failed to further promote Sirt1 expression and inhibit CME formation. MiR-34a-5p contributes to CMD by inhibiting Sirt1 expression. Ligustrazine exerts endothelial-protective, anti-platelet and anti-inflammatory effects to prevent CMD via suppressing miR-34a-5p and promoting Sirt1.

The Uygur herb, Hyssopus officinalis L., has been demonstrated to affect the levels of a number of cytokines in asthmatic mice, including interleukin‑4, ‑6 and ‑17 and interferon‑γ. In the present study, the effect of Hyssopus officinalis L. on airway immune regulation and airway inflammation was investigated in a mouse model of chronic asthma. A total of 32 BALB/c mice were randomly divided into four groups, which included the normal, chronic asthmatic, dexamethasone treatment and Hyssopus officinalis L. treatment groups. Mice were sensitized and challenged with ovalbumin to establish an asthma model and the ratio of eosinophils (EOS) in the bronchoalveolar lavage fluid (BALF) was determined. In addition, the levels of immunoglobulin (Ig)E and IgG were detected using an enzyme‑linked immunosorbent assay. The degree of airway mucus secretion was observed using the periodic acid‑Schiff stain method. The results demonstrated that the ratio of EOS in the BALF and the level of serum IgE in the chronic asthmatic and dexamethasone treatment groups increased, while the level of serum IgG decreased, when compared with the normal group. In addition, excessive secretion of airway mucus was observed in these two groups. However, the EOS ratio in the BALF and the levels of serum IgE and IgG in the Hyssopus officinalis L. treatment group were similar to the results observed in the normal group. In conclusion, Hyssopus officinalis L. not only plays an anti‑inflammatory role by inhibiting the invasion of EOS and decreasing the levels of IgE, but also affects immune regulation.