Linying Jia

Introduction: The new coronavirus has caused a pandemic that has infected hundreds of millions of people around the world since its outbreak. But the cardiovascular damage caused by the new coronavirus is unknown. We have analyzed the current global scenario and the general pattern of growth. After summarizing the known relationship between cardiovascular diseases and new coronary pneumonia, relevant articles are analyzed through bibliometrics and visualization.Methods: Following our pre-designed search strategy, we selected publications on COVID-19 and cardiovascular disease in the Web of Science database. In our relevant bibliometric visualization analysis, a total of 7,028 related articles in the WOS core database up to 20th October 2022 were summarized, and the most prolific authors, the most prolific countries, and the journals and institutions that published the most articles were summarized and quantitatively analyzed.Results: SARS-CoV-2 is more infectious than SARS-CoV-1 and has significant involvement in the cardiovascular system in addition to pulmonary manifestations, with a difference of 10.16% (20.26%/10.10%) in the incidence of cardiovascular diseases. The number of cases increases in winter and decreases slightly in summer with temperature changes, but the increase in cases tends to break out of seasonality across the region as mutant strains emerge. The co-occurrence analysis found that with the progress of the epidemic, the research keywords gradually shifted from ACE2 and inflammation to the treatment of myocarditis and complications, indicating that the research on the new crown epidemic has entered the stage of prevention and treatment of complications.Conclusion: When combined with the current global pandemic trend, how to improve prognosis and reduce human body damage could become a research focus. At the same time, timely detection, prevention, and discovery of new mutant strains have also become key tasks in the fight against the epidemic, and full preparations have been made to prevent the spread of the next wave of mutant strains, and still need to continue to pay attention to the differential performance of the variant “omicron.”

Porcine reproductive and respiratory syndrome virus (PRRSV) induces secretion of high mobility group box 1 (HMGB1) to mediate inflammatory response that is involved in the pulmonary injury of infected pigs. Our previous study indicates that protein kinase C-delta (PKC-delta) is essential for HMGB1 secretion in PRRSV-infected cells. However, the underlying mechanism in HMGB1 secretion induced by PRRSV infection is still unclear. Here, we discovered that the phosphorylation level of HMGB1 in threonine residues increased in PRRSV-infected cells. A site-directed mutagenesis study showed that HMGB1 phosphorylation at threonine-51 was associated with HMGB1 secretion induced by PRRSV infection. Co-immunoprecipitation (co-IP) of HMGB1 failed to precipitate PKC-delta, but interestingly, mass spectrometry analysis of the HMGB1 co-IP product showed that PRRSV infection enhanced HMGB1 binding to ribosomal protein S3 (RPS3), which has various extra-ribosomal functions. The silencing of RPS3 by siRNA blocked HMGB1 secretion induced by PRRSV infection. Moreover, the phosphorylation of HMGB1 at threonine-51 was correlated with the interaction between HMGB1 and RPS3. In vivo, PRRSV infection also increased RPS3 levels and nuclear accumulation in pulmonary alveolar macrophages. These results demonstrate that PRRSV may induce HMGB1 phosphorylation at threonine-51 and increase its interaction with RPS3 to enhance HMGB1 secretion. This finding provides insights into the pathogenesis of PRRSV infection.

Atherosclerosis is a pathological vascular state caused by the interaction of environmental and hereditary factors. Epigenetic modifications may be the bridge connecting environmental factors and genetic factors. A search for publications on the Web of Science database in the field of atherosclerosis related to epigenetics was conducted from the earliest mention to 31 December 2020. Data on total and annual publications, citations, impact factors, Hirsch (H)-index, citation times, most prolific authors, and frequently published journals were collected for quantitative and qualitative comparison. A total of 1848 publications related to epigenetics and atherosclerosis were found. The major contributing countries were the China (522, 28.23%), United States (485, 26.23%), and Germany (119, 6.44%). The greatest number of retrieved publications were published in the journal, “Arteriosclerosis, Thrombosis, and Vascular Biology” (62, 3.66%). The publication “Oxidative Stress and Diabetic Complications” was cited 2370 times. The most frequent keywords were “DNA methylation” and “LncRNA”. Publications on epigenetic research in the atherosclerosis field have increased significantly every year, indicating that the study of epigenetic modifications plays an increasingly important role in understanding the pathology of atherosclerosis.