Thromboinflammation is a critical area of research, particularly in the context of both non-communicable and communicable diseases, with a special emphasis on acute and long COVID. The COVID-19 pandemic has significantly impacted healthcare systems worldwide, challenging existing treatment paradigms and highlighting the need for a deeper understanding of the inflammatory pathways that contribute to endothelial dysfunction and prothrombotic states during SARS-CoV-2 infections. The disease disrupts the delicate balance between platelet interactions and the vessel wall, affecting all components of Virchow’s triad, which includes hypercoagulation in vital organs such as the lungs, heart, and brain. Recent studies have shown that viral persistence and potential reactivation mimic acute infection processes, presenting additional therapeutic challenges. Despite ongoing research, there remains a gap in fully understanding the distinct thromboinflammatory mechanisms at play in COVID-19, necessitating further investigation into these complex interactions.This research topic aims to explore the thromboinflammatory pathways during acute and long COVID, with a particular focus on cardiovascular and respiratory diseases. The objective is to identify and analyze the similarities and differences in pathomechanisms between COVID-19 and other known thromboinflammatory pathways in these diseases. By addressing these distinct differences, the research seeks to enhance our understanding of the role of thromboinflammation in post-COVID sequelae, viral persistence, and the immune system's influence on platelet reactivity during long COVID.To gather further insights into the thromboinflammatory processes in COVID-19, we welcome articles addressing, but not limited to, the following themes:- Thromboinflammation in acute and long COVID- Pathways of thromboinflammation in cardiovascular and respiratory diseases- Role of thromboinflammation in post-COVID sequelae and viral persistence- Role of the immune system in platelet reactivity during long COVID- Immune mechanisms in vascular diseases as a consequence of COVID-19
Thromboinflammation is a critical area of research, particularly in the context of both non-communicable and communicable diseases, with a special emphasis on acute and long COVID. The COVID-19 pandemic has significantly impacted healthcare systems worldwide, challenging existing treatment paradigms and highlighting the need for a deeper understanding of the inflammatory pathways that contribute to endothelial dysfunction and prothrombotic states during SARS-CoV-2 infections. The disease disrupts the delicate balance between platelet interactions and the vessel wall, affecting all components of Virchow’s triad, which includes hypercoagulation in vital organs such as the lungs, heart, and brain. Recent studies have shown that viral persistence and potential reactivation mimic acute infection processes, presenting additional therapeutic challenges. Despite ongoing research, there remains a gap in fully understanding the distinct thromboinflammatory mechanisms at play in COVID-19, necessitating further investigation into these complex interactions.This research topic aims to explore the thromboinflammatory pathways during acute and long COVID, with a particular focus on cardiovascular and respiratory diseases. The objective is to identify and analyze the similarities and differences in pathomechanisms between COVID-19 and other known thromboinflammatory pathways in these diseases. By addressing these distinct differences, the research seeks to enhance our understanding of the role of thromboinflammation in post-COVID sequelae, viral persistence, and the immune system's influence on platelet reactivity during long COVID.To gather further insights into the thromboinflammatory processes in COVID-19, we welcome articles addressing, but not limited to, the following themes:- Thromboinflammation in acute and long COVID- Pathways of thromboinflammation in cardiovascular and respiratory diseases- Role of thromboinflammation in post-COVID sequelae and viral persistence- Role of the immune system in platelet reactivity during long COVID- Immune mechanisms in vascular diseases as a consequence of COVID-19