Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, known as coronavirus disease 2019 (COVID-19) causes cytokine release syndrome (CRS), leading to acute respiratory distress syndrome (ARDS), acute kidney and cardiac injury, liver dysfunction, and multiorgan failure. Although several studies have discussed the role of 5-lipoxygenase (5-LOX) in viral infections, such as influenzae and SARS, it remains unexplored in the pathophysiology of COVID-19. 5-LOX acts on free arachidonic acid (AA) to form proinflammatory leukotrienes (LTs). Of note, numerous cells involved with COVID-19 (e.g., inflammatory and smooth muscle cells, platelets, and vascular endothelium) widely express leukotriene receptors. Moreover, 5-LOX metabolites induce the release of cytokines (e.g., tumour necrosis factor-α [TNF-α], interleukin-1α [IL-1α], and interleukin-1β [IL-1β]) and express tissue factor on cell membranes and activate plasmin. Since macrophages, monocytes, neutrophils, and eosinophils can express lipoxygenases, activation of 5-LOX and the subsequent release of LTs may contribute to the severity of COVID-19. This review sheds light on the potential implications of 5-LOX in SARS-CoV-2-mediated infection and the anticipated therapeutic role of 5-LOX inhibitors.

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染，称为冠状病毒病 2019 (COVID-19)，会导致细胞因子释放综合征 (CRS)，导致急性呼吸窘迫综合征 (ARDS)、急性肾脏和心脏损伤、肝脏功能障碍和多器官功能衰竭。尽管有几项研究讨论了 5-脂氧合酶 (5-LOX) 在流感和 SARS 等病毒感染中的作用，但它在 COVID-19 的病理生理学中仍未得到探索。5-LOX 作用于游离花生四烯酸 (AA) 以形成促炎性白三烯 (LT)。值得注意的是，与 COVID-19 相关的许多细胞（例如炎症细胞和平滑肌细胞、血小板和血管内皮细胞）广泛表达白三烯受体。此外，5-LOX 代谢物诱导细胞因子（例如，肿瘤坏死因子-α [TNF-α]、白介素-1α [IL-1α]、和白细胞介素-1β [IL-1β])，并在细胞膜上表达组织因子并激活纤溶酶。由于巨噬细胞、单核细胞、中性粒细胞和嗜酸性粒细胞可以表达脂氧合酶，因此 5-LOX 的激活和随后 LT 的释放可能导致 COVID-19 的严重程度。这篇综述阐明了 5-LOX 在 SARS-CoV-2 介导的感染中的潜在影响以及 5-LOX 抑制剂的预期治疗作用。