Coronavirus disease 2019 (COVID-19) pandemic is still a world-class challenge. Inflammation, especially its severe form with excess release of pro-inflammatory cytokines (cytokine storm) which is a life-threatening condition, is among the most important suspects involved in COVID-19 pathogenesis. It has been shown that cytokine storm could cause notable morbidities such as acute respiratory distress syndrome (ARDS) which leads to hypoxia which is significantly associated with mortality of patients with COVID-19. Hypoxia-inducible factor 1α (HIF-1α) which activates following ARDS-induced hypoxia plays a crucial role in pathogenesis of cytokine storm. The expression of tumor necrosis factor α (TNF-α), interleukin 1 β (IL-1β), and IL-6 which are key elements of cytokine storm are by nuclear factor κβ (NFκB). Interestingly, during the hypoxia, HIF-1α activates NFκB to induce expression of pro-angiogenic and pro-inflammatory factors. These released factors starts a autocrine/paracrine loop and causes deterioration of their etiological pathways of expression: cytokine storm and ARDS. To sum up, it seems HIF-1α is an important target to hit to ameliorate the mentioned pathways. Herein, we suggest perfluorocarbons (PFCs) which are among the organofluorine compounds as a possible co-treatment to reduce hypoxemia and then hypoxia. These substances are known for their high gas solving potential that make them able to be used as a synthetic artificial blood product. Due to the potential of PFCs to affect the fountain of important physiopathological pathway such as inflammation a hypoxia through affecting NFκB, they could be considered as multi-target co-treatment for ARD individuals with COVID-19. It is highly suggested to evaluate this hypothesis in following researches.

2019 年冠状病毒病 (COVID-19) 大流行仍然是世界级的挑战。炎症，尤其是其严重形式的促炎细胞因子（细胞因子风暴）的过度释放，这是一种危及生命的疾病，是参与 COVID-19 发病机制的最重要的嫌疑人之一。已经表明，细胞因子风暴可能导致显着的发病率，例如导致缺氧的急性呼吸窘迫综合征 (ARDS)，这与 COVID-19 患者的死亡率显着相关。在 ARDS 诱导的缺氧后激活的缺氧诱导因子 1α (HIF-1α) 在细胞因子风暴的发病机制中起着至关重要的作用。细胞因子风暴的关键要素肿瘤坏死因子α (TNF-α)、白细胞介素 1β (IL-1β) 和 IL-6 的表达是由核因子 κβ (NFκB) 表达的。有趣的是，在缺氧期间，HIF-1α 激活 NFκB 以诱导促血管生成和促炎因子的表达。这些释放的因子启动自分泌/旁分泌循环并导致其病因表达途径恶化：细胞因子风暴和 ARDS。综上所述，HIF-1α 似乎是改善上述途径的重要目标。在此，我们建议将有机氟化合物中的全氟化碳 (PFC) 作为可能的联合治疗，以减少低氧血症和缺氧。这些物质以其高气体溶解潜力而闻名，这使它们能够用作合成人造血液产品。由于 PFCs 有可能通过影响 NFκB 来影响重要的病理生理途径的源头，例如炎症和缺氧，它们可以被视为对患有 COVID-19 的 ARD 个体的多目标联合治疗。强烈建议在后续研究中评估这一假设。