Advances in macrophage metabolic reprogramming in myocardial ischemia-reperfusion

被引：1
作者：
Fan, Ao-Di [1 ,2 ]
Lin, Han-qing [1 ,2 ]
Wang, Xi-Zheng [1 ,2 ]
Yang, Ke [1 ,2 ]
Guo, Hong-Xin [3 ]
Zhang, Hai-xia [1 ,2 ]
Fan, Guan-Wei [1 ,2 ]
Li-Lan [1 ,2 ]
机构：
[1] Tianjin Univ Tradit Chinese Med, State Key Lab Modern Chinese Med, Key Lab Pharmacol Tradit Chinese Med Formulae, Minist Educ, Tianjin, Peoples R China
[2] Tianjin Univ Tradit Chinese Med, Teaching Hosp 1, Natl Clin Res Ctr Chinese Med Acupuncture & Moxibu, State Key Lab Component Based Chinese Med, Tianjin, Peoples R China
[3] Henan Univ Tradit Chinese Med, Affiliated Hosp 1, Heart Ctr, Zhengzhou, Peoples R China
来源：
CELLULAR SIGNALLING | 2024年 / 123卷
基金：
中国国家自然科学基金;
关键词：
Macrophage; Myocardial ischemia-reperfusion; Metabolic reprogramming; CARDIAC MACROPHAGES; SUCCINATE-DEHYDROGENASE; LIPID-METABOLISM; DENDRITIC CELLS; STEADY-STATE; INFARCTION; POLARIZATION; PKM2; HIF-1-ALPHA; ACTIVATION;
D O I：
10.1016/j.cellsig.2024.111370
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Acute myocardial infarction (AMI) is the leading cause of death worldwide, and reperfusion therapy is a critical therapeutic approach to reduce myocardial ischemic injury and minimize infarct size. However, ischemia/ reperfusion (I/R) itself also causes myocardial injury, and inflammation is an essential mechanism by which it leads to myocardial injury, with macrophages as crucial immune cells in this process. Macrophages are innate immune cells that maintain tissue homeostasis, host defence during pathogen infection, and repair during tissue injury. During the acute phase of I/R, M1-type macrophages generate a pro-inflammatory milieu, clear necrotic myocardial tissue, and further recruit mononuclear (CCR2+) macrophages. Over time, the reparative (M2 type) macrophages gradually became dominant. In recent years, metabolic studies have shown a clear correlation between the metabolic profile of macrophages and their phenotype and function. M1-type macrophages are mainly characterized by glycolytic energy supply, and their tricarboxylic acid (TCA) cycle and mitochondrial oxidative phosphorylation (OXPHOS) processes are impaired. In contrast, M2 macrophages rely primarily on OXPHOS for energy. Changing the metabolic profile of macrophages can alter the macrophage phenotype. Altered energy pathways are also present in macrophages during I/R, and intervention in this process contributes to earlier and greater M2 macrophage infiltration, which may be a potential target for the treatment of myocardial I/R injury. Therefore, this paper mainly reviews the characteristics of macrophage energy metabolism alteration and phenotypic transition during I/R and its mechanism of mediating myocardial injury to provide a basis for further research in this field.
引用
收藏
页数：11
相关论文
共 111 条
  • [1] Liu J., Zhou Y., Huang H., Liu R., Kang Y., Zhu T., Wu J., Gao Y., Li Y., Wang C., Chen S., Xie N., Zheng X., Meng R., Liu Y., Tan N., Gao F., Impact of stress hyperglycemia ratio on mortality in patients with critical acute myocardial infarction: insight from american MIMIC-IV and the chinese CIN-II study, Cardiovasc. Diabetol., 22, 1, (2023)
  • [2] Ibanez B., James S., Agewall S., Antunes M.J., Bucciarelli-Ducci C., Bueno H., Caforio A.L.P., Crea F., Goudevenos J.A., Halvorsen S., Hindricks G., Kastrati A., Lenzen M.J., Prescott E., Roffi M., Valgimigli M., Varenhorst C., Vranckx P., Widimsky P., ESC Scientific Document Group, 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: the task force for the management of acute myocardial infarction in patients presenting with ST
  • [3] Rabinovich-Nikitin I., Kirshenbaum L.A., Circadian regulated control of myocardial ischemia-reperfusion injury, Trends Cardiovasc. Med., 34, 1, pp. 1-7, (2024)
  • [4] Wei B., Lin Q., Ji Y.G., Zhao Y.C., Ding L.N., Zhou W.J., Zhang L.H., Gao C.Y., Zhao W., Luteolin ameliorates rat myocardial ischaemia-reperfusion injury through activation of peroxiredoxin II, Br. J. Pharmacol., 175, 16, pp. 3315-3332, (2018)
  • [5] Dong Y., Kang Z., Zhang Z., Zhang Y., Zhou H., Liu Y., Shuai X., Li J., Yin L., Wang X., Ma Y., Fan H., Jiang F., Lin Z., Ding C., Yun Jin K., Sarapultsev A., Li F., Zhang G., Xie T., Yin C., Cheng X., Luo S., Liu Y., Hu D., Single-cell profile reveals the landscape of cardiac immunity and identifies a cardio-protective Ym-1hi neutrophil in myocardial ischemia-reperfusion injury, Sci. Bull. (Beijing)., 69, 7, pp. 949-967, (2024)
  • [6] Rurik J.G., Aghajanian H., Epstein J.A., Immune cells and immunotherapy for cardiac injury and repair, Circ. Res., 128, 11, pp. 1766-1779, (2021)
  • [7] Thorp E.B., Cardiac macrophages and emerging roles for their metabolism after myocardial infarction, J. Clin. Invest., 133, 18, (2023)
  • [8] Horckmans M., Ring L., Duchene J., Santovito D., Schloss M.J., Drechsler M., Weber C., Soehnlein O., Steffens S., Neutrophils orchestrate post-myocardial infarction healing by polarizing macrophages towards a reparative phenotype, Eur. Heart J., 38, 3, pp. 187-197, (2017)
  • [9] Choo E.H., Lee J.H., Park E.H., Park H.E., Jung N.C., Kim T.H., Koh Y.S., Kim E., Seung K.B., Park C., Hong K.S., Kang K., Song J.Y., Seo H.G., Lim D.S., Chang K., Infarcted myocardium-primed dendritic cells improve remodeling and cardiac function after myocardial infarction by modulating the regulatory T cell and macrophage polarization, Circulation, 135, 15, pp. 1444-1457, (2017)
  • [10] Weirather J., Hofmann U.D., Beyersdorf N., Ramos G.C., Vogel B., Frey A., Ertl G., Kerkau T., Frantz S., Foxp3+ CD4+ T cells improve healing after myocardial infarction by modulating monocyte/macrophage differentiation, Circ. Res., 115, 1, pp. 55-67, (2014)
12345678910