[1] 中国心血管健康与疾病报告2020概要[J].中国循环杂志,2021,36(6):521-545. [2] Zhu Y, Xian X, Wang Z, et al.Research Progress on the Relationship between Atherosclerosis and Inflammation[J]. Biomolecules,2018,8(3):80. [3] Winkels H,Ehinger E,Ghosheh Y,et al.Atherosclerosis in the single-cell era.[J].Curr Opin Lipidol,2018,5:389-396. [4] Selathurai A,Deswaerte V,Kanellakis P,et al.Natural killer (NK) cells augment atherosclerosis by cytotoxic-dependent mechanisms.[J].Cardiovasc Res,2014,1:128-137. [5] Souilhol C,Harmsen MC,Evans PC,et al.Endothelial-mesenchymal transition in atherosclerosis.[J].Cardiovasc Res,2018,4:565-577. [6] Simionescu M.Implications of early structural-functional changes in the endothelium for vascular disease.[J].Arterioscler Thromb Vasc Biol,2007,2:266-274. [7] Crea F,Libby P.Acute Coronary Syndromes: The Way Forward From Mechanisms to Precision Treatment.[J].Circulation,2017,12:1155-1166. [8] Zhou J,Li YS,Chien S.Shear stress-initiated signaling and its regulation of endothelial function.[J].Arterioscler Thromb Vasc Biol,2014,10:2191-2198. [9] Lluberas N, Trías N, Brugnini A, et al.Lymphocyte subpopulations in myocardial infarction: a comparison between peripheral and intracoronary blood[J].Springerplus. 2015,4:744. [10] Theodorou K,Boon RA.Endothelial Cell Metabolism in Atherosclerosis[J].Front Cell Dev Biol,2022,:82. [11] Nahrendorf M,Swirski FK,Aikawa E,et al.The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions.[J].J Exp Med,2007,12:3037-3047. [12] Mentz RJ,Bakris GL,Waeber B,et al.The past, present and future of renin-angiotensin aldosterone system inhibition.[J].Int J Cardiol,2013,5:1677-1687. [13] Kumric M,Kurir TT,Borovac JA,et al.The Role of Natural Killer (NK) Cells in Acute Coronary Syndrome: A Comprehensive Review[J].Biomolecules,1970,11. [14] Ong SB,Hernández-Reséndiz S,Crespo-Avilan GE,et al.Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities.[J].Pharmacol Ther,2018:73-87. [15] Wang X,Guo Z,Ding Z,et al.Inflammation, Autophagy, and Apoptosis After Myocardial Infarction.[J].J Am Heart Assoc,2018,9. [16] Winkels H,Ley K.Natural Killer Cells at Ease: Atherosclerosis Is Not Affected by Genetic Depletion or Hyperactivation of Natural Killer Cells.[J].Circ Res,2018,1:6-7. [17] Engelbertsen D,Autio A,Verwilligen RAF,et al.Increased lymphocyte activation and atherosclerosis in CD47-deficient mice.[J].Sci Rep,2019,1:10608. [18] Knorr M,Münzel T,Wenzel P.Interplay of NK cells and monocytes in vascular inflammation and myocardial infarction.[J].Front Physiol,2014:295. [19] Bonaccorsi I,Spinelli D,Cantoni C,et al.Symptomatic Carotid Atherosclerotic Plaques Are Associated With Increased Infiltration of Natural Killer (NK) Cells and Higher Serum Levels of NK Activating Receptor Ligands.[J].Front Immunol,2022:1503. [20] Nour-Eldine W,Joffre J,Zibara K,et al.Genetic Depletion or Hyperresponsiveness of Natural Killer Cells Do Not Affect Atherosclerosis Development.[J].Circ Res,2018,1:47-57. [21] Jonasson L,Backteman K,Ernerudh J.Loss of natural killer cell activity in patients with coronary artery disease.[J].Atherosclerosis,2005,2:316-21. [22] Laskarin G,Persic V,Ruzic A,et al.Perforin-mediated cytotoxicity in non-ST elevation myocardial infarction.[J].Scand J Immunol,2011,2:195-204. [23] Backteman K,Ernerudh J,Jonasson L.Natural killer (NK) cell deficit in coronary artery disease: no aberrations in phenotype but sustained reduction of NK cells is associated with low-grade inflammation.[J].Clin Exp Immunol,2014,1:104-112. [24] Hong YJ,Cho YN,Kim TJ,et al.Functional deficiency of natural killer cells in acute coronary syndrome is related to ineffective degranulation.[J].Int J Cardiol,2014,3:613-615. [25] Kumric M,Kurir TT,Borovac JA,et al.The Role of Natural Killer (NK) Cells in Acute Coronary Syndrome: A Comprehensive Review.[J].Biomolecules,1970,11. [26] Aranha FC, Ribeiro U Jr, Basse P, et al.Interleukin-2-activated natural killer cells may have a direct role in the control of Leishmania (Leishmania) amazonensis promastigote and macrophage infection[J]. Scandinavian journal of immunology, 2005, 62(4): 334-341. [27] Ayach BB,Yoshimitsu M,Dawood F,et al.Stem cell factor receptor induces progenitor and natural killer cell-mediated cardiac survival and repair after myocardial infarction.[J].Proc Natl Acad Sci U S A,2006,7:2304-2309. [28] Bouchentouf M,Williams P,Forner KA,et al.Interleukin-2 enhances angiogenesis and preserves cardiac function following myocardial infarction.[J].Cytokine,2011,3:732-738. [29] Yan W,Song Y,Zhou L,et al.Immune Cell Repertoire and Their Mediators in Patients with Acute Myocardial Infarction or Stable Angina Pectoris.[J].Int J Med Sci,2017,2:181-190. [30] Matsumoto K,Obana M,Kobayashi A,et al.Blockade of NKG2D/NKG2D ligand interaction attenuated cardiac remodelling after myocardial infarction.[J].Cardiovasc Res,2019,4:765-775. [31] Wang J,Chen Z,Dai Q,et al.Intravenously delivered mesenchymal stem cells prevent microvascular obstruction formation after myocardial ischemia/reperfusion injury[J].Basic Res Cardiol,2020,4:40. |