[1]王茜 李晶洁.细胞学机制在调控心肌梗死后炎症反应中的研究进展[J].心血管病学进展,2020,(2):190-192.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.023]
 WANG QianLI Jingjie.Cytological Mechanisms in Regulation of The Post-infarction Inflammatory Response[J].Advances in Cardiovascular Diseases,2020,(2):190-192.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.023]
点击复制

细胞学机制在调控心肌梗死后炎症反应中的研究进展()
分享到:

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2020年2期
页码:
190-192
栏目:
综述
出版日期:
2020-02-25

文章信息/Info

Title:
Cytological Mechanisms in Regulation of The Post-infarction Inflammatory Response
作者:
王茜 李晶洁
(哈尔滨医科大学附属第一医院心内科,黑龙江 哈尔滨 150000 )
Author(s):
WANG QianLI Jingjie
(Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin 150000, Heilongjiang, China)
关键词:
心肌梗死炎症反应细胞生物学
Keywords:
Myocardial infarction Inflammatory response Cytological mechanisms
DOI:
10.16806/j.cnki.issn.1004-3934.2020.02.023
摘要:
炎症在心肌梗死后心脏修复中发挥重要作用,适度的炎症反应可以缩小梗死范围,促进缺血心肌的恢复,而持久激活的炎症反应则会加重缺血损伤,引起心脏不良重构。最近研究表明,心肌梗死后炎症和修复细胞的功能超出了传统学说所提出的作用范围。现就梗死后炎症反应的细胞学机制的研究进展做一综述,为进一步研究如何通过调控心肌梗死后的炎症反应从而抑制病理性重构为临床治疗提供新的方向。
Abstract:
Inflammation plays a crucial role in cardiac repair after myocardial infarction. Moderate inflammatory response can reduce the infarct size and promote recovery of ischemic myocardium, while excessive inflammation will aggravate ischemic injury, leading to adverse cardiac remodeling. Recently published studies demonstrated that the functional repertoire of inflammatory and reparative cells may extend beyond the roles suggested by traditional teachings. This review summarizes recent advances in the cytological mechanism of the post-infarction inflammatory response in order to develop new treatment for controling inflammation to suppress pathological remodeling.

参考文献/References:

[1].徐林,陶波.中性粒细胞淋巴细胞比值与急性心肌梗死的相关性研究[J].中国心血管病研究,2017,15(8):257-259.
[2].Frangogiannis NG. The inflammatory response in myocardial injury, repair, and remodelling[J].Nat Rev Cardiol,2014,11(5):255-265.
[3].Saxena A, Russo I, Frangogiannis NG. Inflammation as a therapeutic target in myocardial infarction: learning from past failures to meet future challenges[J].Transl Res,2016, 167(1):152-166.
[4].Pinto AR, Ilinykh A, Ivey MJ, et al. Revisiting cardiac cellular composition[J]. Circ Res, 2015,118(3):400-409.
[5].Chen W, Spitzl A, Mathes DS, et al. Endothelial actions of ANP enhance myocardial inflammatory infiltration in the early phase after acute infarction[J].Circ Res,2016, 119 (2):237-248.
[6].Zhu M, Goetsch S, Wang Z, et al. FoxO4 promotes early inflammatory response upon myocardial infarction via endothelial arg1[J].Circ Res,2015,117(11):967-977.
[7].Entman ML, Youker K,?Shoji T, et al. Neutrophil induced oxidative injury of cardiac myocytes:a compartmented s ystem requiring CD11b/CD18-ICAM-1 adherence[J].J Clin Invest,1992, 90(4):1335-1345.
[8].Horckmans M, Ring L, Duchene J, et al. Neutrophils orchestrate post-myocardial infarction healing by polarizing macrophages towards a reparative phenotype[J]. Eur Heart J,2 016, 38(3):187-197.
[9].Mollenhauer M, Friedrichs K, Lange M, et al. Myeloperoxidase mediates postischemic arrhythmogenic ventricular remodeling[J].Circ Res,2017,121(1):56-70.
[10].Ma Y, Yabluchanskiy A, Iyer RP, et al. Temporal neutrophil polarization following m yocardial infarction[J]. Cardiovasc Res,2016,110(1):51-61.
[11].Hulsmans M, Clauss S, Xiao L, et al. Macrophages facilitateelectrical conduction in the heart[J].Cell, 2017, 169(3):510-522.e20.
[12].Wan E, Yeap XY, Dehn S, et al. Enhanced efferocytosis of apoptoti c cardiomyocytes through myeloid-epithelial-reproductive tyrosine kinase links acute inflammation resolution to cardiac repair after infarction[J]. Circ Res,2013,113(8):1004-1012.
[13].Chen W, Saxena A, Li N, et al. Endogenous IRAK-M attenuates postinfarction remodeling through effects on macrophages and fibroblasts[J].Arterioscler Thromb Vasc Biol,2012, 32(11):2598-2608.
[14].Shiraishi M, Shintani Y, Shintani Y, et al. Alternatively activated macrophages determine repair of the infarcted adult murine heart[J].J Clin Invest, 2016, 126(6):2151.
[15].Howangyin KY, Zlatanova I, Pinto C, et al. Myeloid-epithelial-reproductive receptor tyrosine kinase and milk fat globule epidermal growth factor 8 coordinately improve remodeling after myocardial infarction via local delivery of vascular endothelial growth factor[J].Circulation, 2016,133(9): 826-839.
[16].Frangogiannis NG, Mendoza LH, Lindsey ML, et al. IL-10 is induced in the reperfused myocardium and may modulate the reaction to injury[J].J Immunol,2000, 165(5):2798-2808.
[17].Hofmann U, Frantz S. Role of lymphocytes in myocardial injury, healing, and remodeling after myocardial infarction[J].Circ Res,2015,116(2):354-367.
[18].Dobaczewski M, Xia Y, Bujak M, et al. CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory t cells[J]. Am J Pathol,2010,176(5):2177-2187.
[19].Weirather J, Hofmann UDW, Beyersdorf N, et al.Foxp3+ CD4+ T cells improve healing after myocardial infarction by modulating monocyte/macrophage differentiation[J]. Circ Res,2014,115(1):55-67.
[20].Saxena A, Dobaczewski M, Rai V, et al. Regulatory T cells are recruited in the infarcted mouse myocardium and may modulate fibroblast phenotype and function.[J].Am J Physiol Heart Circ Physiol, 2014, 307(8):H1233.
[21].Ramjee V, Li D, Manderfield LJ, et al. Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarction.[J].J Clin Invest,2017, 127(3):899-911.
[22].Somasundaram P, Ren G, Nagar H, et al. Mast cell tryptase may modulate endothelial cell phe notype in healing myocardial infarcts.[J].J Pathol,2010,205(1): 102-111.
[23].Dewald O, Ren G, Duerr GD, et al. Of mice and dogs: species-specific differences in the inflammatory response following myocardial infarction[J].Am J Pathol, 2004, 164(2):665-677.
[24].Ngkelo A, Richart A,?Kirk JA, et al. Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction [J]. J Experimental Medicine, 2016,213(7):1353-1374.
[25].Katrien VDB, Scott CL, Nindl V, et al. Myocardial infarction primes autoreactive T cells through activation of dendritic cells[J].Cell Reports,2017,18(12): 3005-3017.
[26].Shinde AV, Humeres C, Frangogiannis NG. The role of α-smooth muscle actin in fibroblast-mediated matrix contraction and remodeling[J]. Biochim Biophys Acta, 2017,1863(1):298-309.
[27].Woodall MC, Woodall BP, Gao E,et al. Cardiac fibroblast GRK2 deletion enhances contractility and remodeling following ischemia/reperfusion injury[J].Circ Res,2016,119(10):1116-1127.
[28].Frangogiannis NG.The functional pluralism of fibroblasts in the infarcted myocardium[J]. Circ Res,2016,119(10):1049-1051.
[29].Nakaya M, Watari K, Tajima M, et al. Cardiac myofibroblast engulfment of dead cells facilitates recovery after myocardial infarction [J].J Clin Invest,2016, 127(1):383-401.

相似文献/References:

[1]王铁华,郑景辉,莫云秋.蛋白质组学在心肌梗死中的研究进展[J].心血管病学进展,2015,(5):616.[doi:10.3969/j.issn.1004-3934.2015.05.024]
 WANG Tiehua,ZHENG Jinghui,MO Yunqiu.Research Progress of Proteomics in Myocardial Infarction[J].Advances in Cardiovascular Diseases,2015,(2):616.[doi:10.3969/j.issn.1004-3934.2015.05.024]
[2]王山山 梁兆光.炎症反应与心房颤动的关系[J].心血管病学进展,2019,(5):770.[doi:10.16806/j.cnki.issn.1004-3934.2019.05.026]
 WANG Shanshan,LIANG Zhaoguang.Inflammation and Atrial Fibrillation[J].Advances in Cardiovascular Diseases,2019,(2):770.[doi:10.16806/j.cnki.issn.1004-3934.2019.05.026]
[3]孙洋.基质金属蛋白酶与心肌梗死后心脏重构[J].心血管病学进展,2019,(8):1094.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.006]
 SUN Yang.Matrix Metalloproteinases in Cardiac Remodeling after Myocardial Infarction[J].Advances in Cardiovascular Diseases,2019,(2):1094.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.006]
[4]陈丰 苏强 朱继金.高迁移率族蛋白B1在心脏炎症反应性疾病中的研究进展[J].心血管病学进展,2019,(8):1111.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.010]
 CHEN Feng,SU Qiang,ZHU Jijin.Research Progress of HMGB1 in Myocardial Inflammatory Reactivity Disease[J].Advances in Cardiovascular Diseases,2019,(2):1111.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.010]
[5]常文婧 王丽娜.Hippo通路在心脏发育、再生和疾病中的作用[J].心血管病学进展,2019,(8):1115.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.011]
 CHANG Wenjin,WANG Lina.Role of Hippo Pathway in Heart Development,Regeneration and Disease[J].Advances in Cardiovascular Diseases,2019,(2):1115.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.011]
[6]王宇 周思维 张莎 吴弘.植入型心律转复除颤器在心肌梗死后心脏性猝死中的研究进展[J].心血管病学进展,2020,(1):4.[doi:10.16806/j.cnki.issn.1004-3934.2020.01.002]
 WANG Yu,ZHOU Siwei,ZHANG Sha,et al.Implantable Cardioverter Defibrillator in Sudden Cardiac Death after Myocardial Infarction[J].Advances in Cardiovascular Diseases,2020,(2):4.[doi:10.16806/j.cnki.issn.1004-3934.2020.01.002]
[7]李文松 张润峰.脂蛋白相关磷脂酶与冠心病的相关性研究进展[J].心血管病学进展,2020,(1):85.[doi:10.16806/j.cnki.issn.1004-3934.2020.01.023]
 LI Wensong ZHANG Runfeng.Lipoprotein-associated Phospholipase A2 and Coronary Heart Disease[J].Advances in Cardiovascular Diseases,2020,(2):85.[doi:10.16806/j.cnki.issn.1004-3934.2020.01.023]
[8]位晨晨,钟明.糖尿病心肌病的发病机制[J].心血管病学进展,2020,(2):135.[doi:10.16806/j.cnki.issn.1004-3934.20.02.009]
 WEI Chenchen,ZHONG Ming.Pathogenesis of Diabetic Cardiomyopathy[J].Advances in Cardiovascular Diseases,2020,(2):135.[doi:10.16806/j.cnki.issn.1004-3934.20.02.009]
[9]邹先明 赵然尊.长链非编码RNA ANRIL与心血管疾病的研究进展[J].心血管病学进展,2020,(2):167.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.017]
 ZOU Xianming,ZHAO Ranzun.Long Non-Coding RNA ANRIL and Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2020,(2):167.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.017]
[10]黄柳,张瑞宁,田小超,等.内皮祖细胞与冠心病患者CD14CD16+单核细胞共培养后移植心肌梗死大鼠对血管密度及心肌梗死面积的影响[J].心血管病学进展,2020,(2):203.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.027]
 HUANG Liu,ZHANG Ruining,TIAN Xiaochao,et al.Effects of Co-cultured Endothelial Progenitor Cells and CD14++CD16+ Monocytes from Coronary Heart Disease Patients on Vascular Density and Myocardial Infarction Size in Transplanting Myocardial Infarction Rats[J].Advances in Cardiovascular Diseases,2020,(2):203.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.027]
[11]张彩霞 曾彬 廖小婷.心肌梗死模型中三碘甲状腺原氨酸对心肌的保护作用研究[J].心血管病学进展,2020,(11):1209.[doi:10.16806/j.cnki.issn.1004-3934.20.11.000]
 ZHANG Caixia,ZENG Bin,LIAO Xiaoting.Protective Effect of Triiodothyronine on Myocardium in Myocardial Infarction Model[J].Advances in Cardiovascular Diseases,2020,(2):1209.[doi:10.16806/j.cnki.issn.1004-3934.20.11.000]
[12]张国贤 彭瑜 张钲.冠状动脉内皮细胞线粒体损伤在心肌梗死中的研究进展[J].心血管病学进展,2023,(3):203.[doi:10.16806/j.cnki.issn.1004-3934.2023.03.003]
 ZHANG Guoxian,PENG Yu,ZHANG Zheng.Mitochondrial Injury of Coronary Endothelial Cells in Myocardial Infarction[J].Advances in Cardiovascular Diseases,2023,(2):203.[doi:10.16806/j.cnki.issn.1004-3934.2023.03.003]
[13]李铭,高继先,吴冰,等.卡格列净减轻心肌梗死后细胞凋亡及炎症反应改善预后[J].心血管病学进展,2024,(4):368.[doi:10.16806/j.cnki.issn.1004-3934.2024.04.018]
 LI Ming,GAO Jixian,WU Bing,et al.Canagliflozin alleviates apoptosis and inflammation after myocardial infarction, and improves prognosis[J].Advances in Cardiovascular Diseases,2024,(2):368.[doi:10.16806/j.cnki.issn.1004-3934.2024.04.018]

更新日期/Last Update: 2020-04-14