ICA69 aggravates ferroptosis causing septic cardiac dysfunction via STING trafficking

• Published in: Cell death discovery Vol. 8; no. 1; pp. 187 - 13
• Main Authors: Kong, Chang, Ni, Xuqing, Wang, Yixiu, Zhang, Anqi, Zhang, Yingying, Lin, Feihong, Li, Shan, Lv, Ya, Zhu, Jingwen, Yao, Xinyu, Dai, Qinxue, Mo, Yunchang, Wang, Junlu
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 09.04.2022; Springer Nature B.V; Nature Publishing Group
• Subjects: 4-Hydroxynonenal; 631/250/1933; 631/250/256; 631/80/82; Apoptosis; Biochemistry; Biomedical and Life Sciences; Cardiac muscle; Cardiomyocytes; Cardiomyopathy; Cardiovascular diseases; Cell Biology; Cell Cycle Analysis; Ferroptosis; Glutathione peroxidase; ICA1 protein; Immune response; Inflammation; Leukocytes (mononuclear); Life Sciences; Lipid peroxidation; Lipopolysaccharides; Macrophages; Malondialdehyde; Prostaglandin endoperoxide synthase; Prostaglandin endoperoxide synthase 2; Reactive oxygen species; Sepsis; Stem Cells; Superoxide dismutase

Previous studies have demonstrated that cardiomyocyte apoptosis, ferroptosis, and inflammation participate in the progress of sepsis-induced cardiomyopathy (SIC). Although Islet cell autoantigen 69 (ICA69) is an imperative molecule that could regulate inflammation and immune response in numerous ill...