International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(3), С. 874 - 874
Опубликована: Янв. 21, 2025
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a disease that can range in presentation from mild symptoms to severe conditions such as pneumonia and distress syndrome. SARS-CoV-2, single-stranded RNA virus, spreads through aerosols droplets. It enters human cells by binding the angiotensin-converting enzyme receptor, leading various complications, including significant alterations red blood potential disruptions haemoglobin function oxygen transport. During infection, interaction between hypoxia, inflammation, haematopoiesis affects erythropoiesis at multiple levels. Hypoxia resulting lung complications reduced cell count, influence regulation of hepcidin, key regulator iron levels blood. Elevated hepcidin are associated with hypoxia suppression erythroferrone, hormone normally inhibits production. Despite high patients intensive care units often exhibit elevated ferritin levels, which, rather than indicating low suggest disrupted metabolism development anaemia. Iron is kept stores, likely due paradoxically which explains measurements. An increase immature decrease CD71+ erythroid observed. The highlight their dual role modulating hyper-inflammation immune response during progression. This review examines pathway SARS-CoV-2 production haematopoietic system how it triggers cytokine storms interleukins, cells, cells. Understanding these processes provides novel pathways for managing haematological manifestations responses COVID-19.
Язык: Английский