巨噬细胞极化
巨噬细胞
心室重构
心肌梗塞
内科学
M2巨噬细胞
医学
化学
体外
生物化学
作者
Xiyi Lu,Qingwei Ji,Heng Pan,Yuncong Feng,Di Ye,Liren Gan,Jun Wan,Jing Ye
标识
DOI:10.1016/j.bcp.2024.116072
摘要
Interleukin-23p19 (IL-23p19) has been demonstrated to be involved in the occurrence and development of cardiovascular diseases such as myocardial infarction and atherosclerosis. This study aimed to examine whether IL-23p19 regulates cardiac remodeling processes and explore its possible mechanisms. Transverse aortic constriction was performed to construct a mouse cardiac remodeling model, and sham surgery was used as a control. The results showed that IL-23p19 expression was increased in the heart after surgery and may be mainly produced by cardiac macrophages. Knockout of IL-23p19 attenuated M1 macrophage polarization, reduced ferroptosis, improved the process of cardiac remodeling and alleviated cardiac dysfunction in TAC mice. Cell culture experiments found that macrophages were the main cause of ferroptosis when phenylephrine (PE) was added, and blocking ferroptosis with ferrostatin-1 (Fer-1), a ferroptosis inhibitor, significantly inhibited M1 macrophage polarization. Treatment with Fer-1 also improved cardiac remodeling and alleviated cardiac dysfunction in IL-23p19-/- mice subjected to TAC surgery. Finally, TAC IL-23p19-/- mice that were administered macrophages isolated from WT mice exhibited an increased proportion of M1 macrophages and aggravated cardiac remodeling, and these effects were reversed when Fer-1 was administered. Knockout of IL-23p19 may attenuate M1 macrophage polarization to improve the cardiac remodeling process by reducing macrophage ferroptosis, and IL-23p19 may be a potential target for the prevention and treatment of cardiac remodeling.
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