Dear All,

I am happy to greet all readers, editors, reviewers, staff members and publishers of SBPR on the eve of year 2022. I thank all of you for your efforts in creating this journal and making it work despite all the challenges faced by a new independent journal in the age dominated by huge publishers, research societies and citation systems. Please accept my best wishes for the year 2022 in your professional and personal undertakings!

Immune thrombocytopenia (ITP) is an acquired bleeding disorder of autoimmune pathophysiology. The causes of ITP could be related to other pathology (viral, bacterial, or systemic), or ITP could develop without any apparent reason. While the immune system dysregulation mechanisms in ITP were described, its etiology remains unclear. Moreover, all existing treatment approaches are not specific for ITP, and its action is highly patient- specific. Here we describe recent findings in the origins and development of ITP and discuss novel experimental and theoretical approaches to diagnosing ITP and predicting therapy effects.

Small, non-nuclear cells, platelets, are primarily designed to form aggregates when blood vessels are damaged, stopping bleeding. To perform this function, platelets can implement several functional responses induced by various agonists and coordinated by a complex network of intracellular signaling triggered by a dozen of different receptors. This review, the second in a series, describes the known intracellular signaling pathways induced by platelet receptors in response to canonical and rare agonists. Particular focus will be on interaction points and “synergy” of platelet activation pathways and intermediate or “secondary” activation mediators that transmit a signal to functional manifestations.

It is known that in COVID-19, hypercoagulation and sometimes thrombocytopenia are related to disease severity. There is also controversial data on platelet participation in COVID-19 pathology. We aimed to determine the degree of platelet hyperactivation in COVID-19 patients. Whole blood flow cytometry with Annexin-V and lactadherin staining ("PS+ platelets") was utilized. Additionally, a stochastic mathematical model of platelet production and consumption was developed. Here we demonstrated that the percentage of PS+ platelets in COVID-19 patients was twofold that of healthy donors. There was a significant correlation between the amount of PS+ platelets and the percentage of lung damage in patients. No connection was found between platelet senescence and hospital therapy or patients' chronic diseases, except for chronic lung disease. Although no thrombocytopenia was observed in patients, the observed increase in platelet size (FSC-A parameter in flow cytometry) could indicate that platelet age is decreased in patients. The developed computational model of platelet turnover confirms the possibility of intense platelet consumption without noticeable changes in platelet count. We conclude that the observed platelet hyperactivation in COVID-19 could be caused by platelet activation in circulation, leading to platelet consumption without significant thrombocytopenia.