白细胞介素-13衍生的2型固有淋巴细胞通过信号转导和转录激活因子3信号通路改善心肌细胞凋亡。
IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway.
作者信息
Hong Ting, Li Saiqi, Guo Xiaoyu, Wei Yazhong, Zhang Jingjing, Su Xiaohui, Zhou Miao, Jin Haizhen, Miao Qing, Shen Lei, Zhu Minfang, He Bin
机构信息
Department of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
出版信息
Front Cell Dev Biol. 2021 Sep 20;9:742662. doi: 10.3389/fcell.2021.742662. eCollection 2021.
The involvement of cardiomyopathy during sepsis means higher mortality and prolonged length of hospital stay. Many efforts have been made to alleviate the apoptosis of cardiomyocytes in sepsis. The huge potential of IL-13 in tissue repair has attracted increasing attention. In the present study, we used LPS-treated mice or primary cardiomyocytes as a sepsis model to explore the anti-apoptotic ability of IL-13. It was found that an increased level of exogenous IL-13 was beneficial to the recovery of heart function in sepsis, and this anti-apoptotic effect of IL-13 was probably through enhancing the phosphorylation of STAT3 Ser727. In addition, we identified that the heart protective effect of IL-13 was associated with type 2 innate lymphocytes (ILC2). All these findings may provide a potential promising treatment for sepsis-induced cardiomyopathy.
脓毒症期间心肌病的发生意味着更高的死亡率和更长的住院时间。人们已经做出了许多努力来减轻脓毒症中心肌细胞的凋亡。IL-13在组织修复中的巨大潜力已引起越来越多的关注。在本研究中，我们使用脂多糖处理的小鼠或原代心肌细胞作为脓毒症模型，以探索IL-13的抗凋亡能力。研究发现，外源性IL-13水平的升高有利于脓毒症中心脏功能的恢复，并且IL-13的这种抗凋亡作用可能是通过增强STAT3 Ser727的磷酸化来实现的。此外，我们还确定IL-13的心脏保护作用与2型固有淋巴细胞（ILC2）有关。所有这些发现可能为脓毒症诱导的心肌病提供一种潜在的有前景的治疗方法。
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