Background. Ferroptosis is a type of cell death with major topic of debate under current research and plays an important role in disease regulation. Objective. In this study, the literature management software Bibexcel and knowledge graph tool VOSviewer were used to summarize and analyze the international research trends and hotspots about ferroptosis in recent years, which highlight the disease mechanism, diagnosis, and treatment related to ferroptosis. Material/Methods. The core collection database of Web of Science was used for retrieving ferroptosis research literature. The information such as the amount of text, the country, the period, the institution, the fund, and the keywords was extracted by the bibliometric tool Bibexcel. The cooccurrence and clustering function of VOSviewer were used to analyze the high-frequency keywords and the cooperative network of the author, institution, and country. Results. The research of ferroptosis started late and was formally proposed in 2012. It has developed rapidly and presented an exponential growth trend. China, the United States, Germany, Japan, and France are the main national forces of ferroptosis research development. The United States and China have a relatively high degree of support and attention to ferroptosis. Exploring oxidative stress, inducers/inhibitors, synergistic antitumor effect, relationships with other cell death types, GSH/GPX4 and iron metabolism imbalance related mechanisms of ferroptosis, and ferroptosis in the nervous system disease, ischemia-reperfusion injury, tumor, inflammation, and age-related diseases are the hot research directions. Conclusion. Ferroptosis has been a research hotspot in the field of biomedicine in recent years and has attracted the attention of scholars all over the world. The occurrence mechanism of ferroptosis and its application in neurological diseases, ischemia and reperfusion injury, tumors, inflammation, and aging are the hot directions of current research. In the future, ferroptosis can be appropriately considered for strengthening new approaches, new diseases, new inductors, new inhibitors, clinical transformation, and traditional medicine research.

Background: Myocardial ischemia-reperfusion injury (MIRI) presents a significant challenge to the effectiveness of reperfusion therapy in severe ischemic heart disease. One of the core pathological mechanisms of MIRI is NLRP3 inflammasome-mediated cardiomyocyte pyroptosis. While electroacupuncture (EA) has demonstrated efficacy in mitigating MIRI, its potential to target and inhibit NLRP3 inflammasome-mediated cardiomyocyte pyroptosis in the context of MIRI remains unclear. Additionally, the mechanism through which local EA may remotely influence the heart to alleviate MIRI is not well understood. Objective: This study aims to explore the protective effects and molecular mechanisms of EA targeting NLRP3 inflammasome-mediated myocardial cell death in MIRI, focusing on the role of serum exosomes. Methods and results: An animal model of MIRI was established by ligating the left anterior descending coronary artery, and EA was applied at the Neiguan (PC6) acupoint. Cardiac function, myocardial infarction area, serum myocardial enzymes, inflammatory factors, and myocardial cell pathological changes were assessed using echocardiography, Evans-TTC staining, ELISA, and H&E staining to confirm the therapeutic effect of EA in reducing MIRI. The NLRP3 agonist Nigericin was applied, and the expression levels of key genes and proteins related to NLRP3-mediated apoptosis were measured by Western blotting and RT-qPCR, confirming that EA alleviates MIRI by targeting and inhibiting NLRP3-mediated myocardial apoptosis. The role of serum exosomes in inhibiting NLRP3 inflammasome-mediated cardiomyocyte pyroptosis was then tested in a cardiomyocyte hypoxia/reoxygenation model. Exosomes from serum samples of AMI-PCI patients (with or without standard EA) and from MIRI model rats were isolated. Small RNA sequencing was performed to identify key effector miRNAs post-EA. Our findings revealed that miR-22-3p was significantly upregulated in serum exosomes following EA. Further validation demonstrated that miR-22-3p mitigates MIRI by targeting NLRP3 to inhibit cardiomyocyte pyroptosis, as confirmed through target gene prediction, in vitro cell experiments, and in vivo animal studies. Conclusion: This study provides evidence that EA reduces MIRI by upregulating miR-22-3p in serum exosomes, which in turn targets and inhibits NLRP3 inflammasome-mediated cardiomyocyte pyroptosis, thereby reducing severe myocardial injury.