Wang Hao, Rouhi Nadiyeh, Slotabec Lily A, Seale Blaise C, Wen Changhong, Filho Fernanda, Adenawoola Michael I, Li Ji
Department of Physiology and Biophysics, Mississippi Center for Heart Research, University of Mississippi Medical Center, Jackson, MS 39216, USA.
G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS 39216, USA.
Life (Basel). 2024 Aug 5;14(8):981. doi: 10.3390/life14080981.
Ischemic heart disease, manifesting as myocardial infarction (MI), remains the leading cause of death in the western world. Both ischemia and reperfusion (I/R) cause myocardial injury and result in cardiac inflammatory responses. This sterile inflammation in the myocardium consists of multiple phases, involving cell death, tissue remodeling, healing, and scar formation, modulated by various cytokines, including the macrophage migration inhibitory factor (MIF). Meanwhile, different immune cells participate in these phases, with myeloid cells acting as first responders. They migrate to the injured myocardium and regulate the initial phase of inflammation. The MIF modulates the acute inflammatory response by affecting the metabolic profile and activity of myeloid cells. This review summarizes the role of the MIF in regulating myeloid cell subsets in MI and I/R injury and discusses emerging evidence of metabolism-directed cellular inflammatory responses. Based on the multifaceted role of the MIF affecting myeloid cells in MI or I/R, the MIF can be a therapeutic target to achieve metabolic balance under pathology and alleviate inflammation in the heart.
缺血性心脏病，表现为心肌梗死（MI），仍然是西方世界的主要死因。缺血和再灌注（I/R）都会导致心肌损伤并引发心脏炎症反应。心肌中的这种无菌性炎症由多个阶段组成，涉及细胞死亡、组织重塑、愈合和瘢痕形成，受到多种细胞因子的调节，包括巨噬细胞迁移抑制因子（MIF）。同时，不同的免疫细胞参与这些阶段，髓系细胞作为第一反应者。它们迁移到受损心肌并调节炎症的初始阶段。MIF通过影响髓系细胞的代谢谱和活性来调节急性炎症反应。本综述总结了MIF在调节MI和I/R损伤中的髓系细胞亚群方面的作用，并讨论了代谢导向的细胞炎症反应的新证据。基于MIF在MI或I/R中对髓系细胞的多方面作用，MIF可以成为在病理状态下实现代谢平衡和减轻心脏炎症的治疗靶点。
