Hojyo Shintaro, Uchida Mona, Tanaka Kumiko, Hasebe Rie, Tanaka Yuki, Murakami Masaaki, Hirano Toshio
Molecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.
Headquarters, National Institutes for Quantum and Radiological Science and Technology, Chiba, 263-8555 Japan.
Inflamm Regen. 2020 Oct 1;40:37. doi: 10.1186/s41232-020-00146-3. eCollection 2020.
The newly emerging coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in Wuhan, China, but has rapidly spread all over the world. Some COVID-19 patients encounter a severe symptom of acute respiratory distress syndrome (ARDS) with high mortality. This high severity is dependent on a cytokine storm, most likely induced by the interleukin-6 (IL-6) amplifier, which is hyper-activation machinery that regulates the nuclear factor kappa B (NF-κB) pathway and stimulated by the simultaneous activation of IL-6-signal transducer and activator of transcription 3 (STAT3) and NF-κB signaling in non-immune cells including alveolar epithelial cells and endothelial cells. We hypothesize that IL-6-STAT3 signaling is a promising therapeutic target for the cytokine storm in COVID-19, because IL-6 is a major STAT3 stimulator, particularly during inflammation. We herein review the pathogenic mechanism and potential therapeutic targets of ARDS in COVID-19 patients.
由严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引起的新型冠状病毒病2019（COVID-19）最初在中国武汉被报道，但已迅速在全球传播。一些COVID-19患者会出现严重的急性呼吸窘迫综合征（ARDS）症状，死亡率很高。这种高严重性取决于细胞因子风暴，很可能是由白细胞介素-6（IL-6）放大器诱导的，它是一种调节核因子κB（NF-κB）途径的过度激活机制，并在包括肺泡上皮细胞和内皮细胞在内的非免疫细胞中由IL-6信号转导和转录激活因子3（STAT3）与NF-κB信号的同时激活所刺激。我们假设IL-6-STAT3信号传导是COVID-19中细胞因子风暴的一个有前景的治疗靶点，因为IL-6是主要的STAT3刺激因子，尤其是在炎症期间。我们在此综述COVID-19患者中ARDS的发病机制和潜在治疗靶点。
