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心肌梗死中涉及炎症和凋亡的机制

姜舒 芮耀诚 李铁军

姜舒, 芮耀诚, 李铁军. 心肌梗死中涉及炎症和凋亡的机制[J]. 药学实践与服务, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007
引用本文: 姜舒, 芮耀诚, 李铁军. 心肌梗死中涉及炎症和凋亡的机制[J]. 药学实践与服务, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007
JIANG Shu, RUI Yaocheng, Li Tiejun. The mechanisms of inflammation and apoptosis in myocardial infarction[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007
Citation: JIANG Shu, RUI Yaocheng, Li Tiejun. The mechanisms of inflammation and apoptosis in myocardial infarction[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007

心肌梗死中涉及炎症和凋亡的机制

doi: 10.3969/j.issn.1006-0111.2016.02.007

The mechanisms of inflammation and apoptosis in myocardial infarction

  • 摘要: 由心肌梗死引起的炎症反应和细胞凋亡对病程的发展和预后有着极其重要的作用,炎症可以通过肿瘤坏死因子α(TNF-α)、CCAAT/增强子结合蛋白同源蛋白(CHOP)、白细胞介素10(IL-10)、α7烟酸型乙酰胆碱受体(α7nAChR)信号途径对细胞的凋亡进行调控,凋亡反馈可影响炎症的严重程度,两者共同影响了心肌梗死面积的大小和心功能的恢复。抑制炎症和减少凋亡已经成为心肌梗死后预防心室重构、调节心功能紊乱的重要环节,对其深入研究具有广阔的前景。
  • [1] Kajstura J, Cheng W, Reiss K, et al. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats[J]. Lab Invest, 1996, 74(1):86-107.
    [2] Roy S, Khanna S, Kuhn DE, et al. Transcriptome analysis of the ischemia-reperfused remodeling myocardium:temporal changes in inflammation and extracellular matrix[J]. Physiol Genom, 2006, 25(3):364-374.
    [3] van den Akker F, Deddens JC, Doevendans PA, et al. Cardiac stem cell therapy to modulate inflammation upon myocardial infarction[J]. Biochem Biophys Acta, 2013, 1830(2):2449-2458.
    [4] Arslan F, de Kleijn DP, Pasterkamp G. Innate immune signaling in cardiac ischemia[J]. Nat Rev Cardiol, 2011,8(5):292-300.
    [5] Chen C, Feng Y, Zou L, et al. Role of extracellular RNA and TLR3-Trif signaling in myocardial ischemia-reperfusion injury[J]. J Am Heart Assoc, 2014, 3(1):e000683.
    [6] Liehn EA, Merx MW, Postea O, et al. Ccr1 deficiency reduces inflammatory remodelling and preserves left ventricular function after myocardial infarction[J]. J Cell Mol Med, 2008, 12(2):496-506.
    [7] Chello M, Anselmi A, Spadaccio C, et al. Simvastatin increases neutrophil apoptosis and reduces inflammatory reaction after coronary surgery[J]. Ann Thorac Surg, 2007, 83(4):1374-1380.
    [8] Buyukkaya E, Poyraz F, Karakas MF, et al. Usefulness of monocyte chemoattractant protein-1 to predict no-reflow and three-year mortality in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention[J]. Am J Cardiol, 2013, 112(2):187-193.
    [9] Dong F, Harvey J, Finan A, et al. Myocardial CXCR4 expression is required for mesenchymal stem cell mediated repair following acute myocardial infarction[J]. Circulation, 2012, 126(3):314-324.
    [10] Miller EJ, Li J, Leng L, et al. Macrophage migration inhibitory factor stimulates AMP-activated protein kinase in the ischaemic heart[J]. Nature, 2008, 451(7178):578-582.
    [11] Gao XM, Liu Y, White D, et al. Deletion of macrophage migration inhibitory factor protects the heart from severe ischemia-reperfusion injury:a predominant role of anti-inflammation[J]. J Mol Cell Cardiol, 2011, 50(6):991-999.
    [12] Bradley JR. TNF-mediated inflammatory disease[J]. J Pathol, 2008, 214(2):149-160.
    [13] Peter ME, Krammer PH. The CD95(APO-1/Fas) DISC and beyond[J]. Cell Death Differ, 2003, 10(1):26-35.
    [14] Zhang R, Xu Y, Ekman N, et al. Etk/Bmx transactivates vascular endothelial growth factor 2 and recruits phosphatidylinositol 3-kinase to mediate the tumor necrosis factor-induced angiogenic pathway[J]. J Biol Chem, 2003,278(51):51267-51276.
    [15] Miyazaki Y, Kaikita K, Endo M, et al. C/EBP homologous protein deficiency attenuates myocardial reperfusion injury by inhibiting myocardial apoptosis and inflammation[J]. Arterioscler Thromb Vasc Biol, 2011, 31(5):1124-1132.
    [16] Oyadomari S, Mori M. Roles of CHOP/GADD153 in endoplasmic reticulum stress[J]. Cell Death Differ, 2004, 11(4):381-389.
    [17] Li Y, Schwabe RF, DeVries-Seimon T, et al. Free cholesterol-loaded macrophages are an abundant source of tumor necrosis factor-a and interleukin-6:model of NF-kappaB-and map kinase-dependent inflammation in advanced atherosclerosis[J]. J Biol Chem, 2005, 280(23):21763-21772.
    [18] Krishnamurthy P, Lambers E, Verma S, et al. Myocardial knockdown of mRNA-stabilizing protein HuR attenuates post-MI inflammatory response and left ventricular dysfunction in IL-10-null mice[J]. FASEB J, 2010, 24(7):2484-2494.
    [19] Krishnamurthy P, Rajasingh J, Lambers E, et al. IL-10 inhibits inflammation and attenuates left ventricular remodeling after myocardial infarction via activation of STAT3 and suppression of HuR[J]. Circ Res, 2009, 104(2):e9-18.
    [20] Zhao M, He X, Bi XY, et al. Vagal stimulation triggers peripheral vascular protection through the cholinergic anti-inflammatory pathway in a rat model of myocardial ischemia/reperfusion[J]. Basic Res Cardiol, 2013, 108(3):345.
    [21] Kakinuma Y, Ando M, Kuwabara M, et al. Acetylcholine from vagal stimulation protects cardiomyocytes against ischemia and hypoxia involving additive non-hypoxic induction of HIF-1alpha[J]. FEBS Lett, 2005, 579(10):2111-2118.
    [22] Ottani A, Giuliani D, Galantucci M, et al. Melanocortins counteract inflammatory and apoptotic responses to prolonged myocardial ischemia/reperfusion through a vagus nerve-mediated mechanism[J]. Eur J Pharmacol, 2010, 637(1-3):124-130.
    [23] Takai S, Jin D, Miyazaki M. Multiple mechanisms for the action of chymase inhibitors[J]. J Pharmacol Sci, 2012, 118(3):311-316.
    [24] Oyamada S, Bianchi C, Takai S, et al. Chymase inhibition reduces infarction and matrix metalloproteinase-9 activation and attenuates inflammation and fibrosis after acute myocardial ischemia/reperfusion[J]. J Pharmacol Exp Ther, 2011, 339(1):143-151.
    [25] Chao J, Chao L. Kallikrein-kinin in stroke, cardiovascular and renal disease[J]. Exp Physiol, 2005, 90(3):291-298.
    [26] Chao J, Yin H, Gao L, et al. Tissue kallikrein elicits cardioprotection by direct kinin b2 receptor activation independent of kinin formation[J]. Hypertension, 2008, 52(4):715-720.
    [27] Stadnicki A. Intestinal tissue kallikrein-kinin system in inflammatory bowel disease[J]. Inflamm Bowel Dis, 2011, 17(2):645-654.
    [28] Yao YY, Yin H, Shen B, et al. Tissue kallikrein infusion prevents cardiomyocyte apoptosis, inflammation and ventricular remodeling after myocardial infarction[J]. Regul Pept, 2007, 140(1-2):12-20.
    [29] Rodrigo R, Prieto JC, Castillo R. Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n-3 fatty acids:molecular mechanisms and potential clinical applications[J]. Clin Sci, 2013, 124(1):1-15.
    [30] Oropeza M, Petersen B, Carnwath JW, et al. Transgenic expression of the human A20 gene in cloned pigs provides protection against apoptotic and inflammatory stimuli[J]. Xenotransplantation, 2009, 16(6):522-534.
    [31] Hunt DL, Campbell PH, Zambon AC, et al. Early postmyocardial infarction survival in Murphy Roths Large mice is mediated by attenuated apoptosis and inflammation but depends on genetic background[J]. Exp Physiol, 2012, 97(1):102-114.
    [32] Meybohm P, Gruenewald M, Albrecht M, et al. Hypothermia and postconditioning after cardiopulmonary resuscitation reduce cardiac dysfunction by modulating inflammation, apoptosis and remodeling[J]. PLoS ONE, 2009, 4(10):e7588.
    [33] Diepenhorst GM, Ciurana CL, Diaz Padilla N, et al. IgM antibodies against apoptotic cells and phosphorylcholine in patients with acute myocardial infarction in relation to infarct size and inflammatory response[J]. Adv Clin Exp Med, 2012, 21(4):455-467.
    [34] Vincent A, Lattuca B, Merlet N, et al. New insights in research about acute ischemic myocardial injury and inflammation[J]. Antiinfl Antialler Agents Med Chem, 2013, 12(1):47-54.
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  • 收稿日期:  2014-03-13
  • 修回日期:  2015-06-01

心肌梗死中涉及炎症和凋亡的机制

doi: 10.3969/j.issn.1006-0111.2016.02.007

摘要: 由心肌梗死引起的炎症反应和细胞凋亡对病程的发展和预后有着极其重要的作用,炎症可以通过肿瘤坏死因子α(TNF-α)、CCAAT/增强子结合蛋白同源蛋白(CHOP)、白细胞介素10(IL-10)、α7烟酸型乙酰胆碱受体(α7nAChR)信号途径对细胞的凋亡进行调控,凋亡反馈可影响炎症的严重程度,两者共同影响了心肌梗死面积的大小和心功能的恢复。抑制炎症和减少凋亡已经成为心肌梗死后预防心室重构、调节心功能紊乱的重要环节,对其深入研究具有广阔的前景。

English Abstract

姜舒, 芮耀诚, 李铁军. 心肌梗死中涉及炎症和凋亡的机制[J]. 药学实践与服务, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007
引用本文: 姜舒, 芮耀诚, 李铁军. 心肌梗死中涉及炎症和凋亡的机制[J]. 药学实践与服务, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007
JIANG Shu, RUI Yaocheng, Li Tiejun. The mechanisms of inflammation and apoptosis in myocardial infarction[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007
Citation: JIANG Shu, RUI Yaocheng, Li Tiejun. The mechanisms of inflammation and apoptosis in myocardial infarction[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007
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