Cyr61、RIPK3与冠状动脉性心脏病的研究进展

人杰 钱(承德医学院附属医院，中国)
振江 丁(承德医学院附属医院，中国)

摘要

近期研究均提示富含半胱氨酸蛋白61（cysteine-rich angiogenic inducer 61，Cyr61）、受体相互作用蛋白激酶3（receptor-interacting protein kinase 3，RIPK3）与冠状动脉性心脏病（coronary heart disease，CHD）的诊断、预测病变的严重程度及预后情况具有一定联系。论文通过对Cyr61、RIPK3与CHD的相关性研究进行总结，期望为CHD的早期诊断及治疗提供新的方向。

关键词

冠状动脉性心脏病；富含半胱氨酸蛋白61；受体相互作用蛋白激酶3

参考

国家心血管病中心.中国心血管健康与疾病报告2020[J].心肺血管病杂志,2021(10):1005-1009.

Garg P, Morris P, Fazlanie AL, et al. Cardiac biomarkers of acute coronary syndrome: From history to high-sensitivity cardiac troponin[J]. Intern Emerg Med,2017(12):147-155.

Kavsak PA, MacRae AR, Lustig V, et al. The impact of the ESC/ACC redefinition of myocardial infarction and new sensitive troponin assays on the frequency of acute myocardial infarction[J]. Am Heart J,2006(152):118-125.

Perbal B, Tweedie S, Bruford E. The official unified nomenclature adopted by the HGNC calls for the use of the acronyms, CCN1-6, and discontinuation in the use of CYR61, CTGF, NOV and WISP 1-3 respectively[J]. J Cell Commun Signal,2018(12): 625-629.

Leask A, Abraham DJ. All in the CCN family: essential matricellular signaling modulators emerge from the bunker[J]. J Cell Sci ,2006(119):4803-4810.

Imhof BA, Jemelin S, Ballet R, et al. CCN1/CYR61-mediated meticulous patrolling by Ly6Clow monocytes fuels vascular inflammation[J]. Proc Natl Acad Sci U S A,2016,113(33):4847-4856.

Chaqour B. Regulating the regulators of angiogenesis by CCN1 and taking it up a Notch[J]. J Cell Commun Signal, 2016 Sep,10(3):259-261.

Yu Y, Gao Y, Qin J, et al. CCN1 promotes the differentiation of endothelial progenitor cells and reendothelialization in the early phase after vascular injury[J]. Basic Res Cardiol,2010 ,105(6):

-24.

Hinkel R, Trenkwalder T, Petersen B, et al. MRTF-A controls vessel growth and maturation by increasing the expression of CCN1 and CCN2[J]. Nat Commun,2014(5):3970.

Choi C, Jeong W, Ghang B, et al. Cyr61 synthesis is induced by interleukin-6 and promotes migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis[J]. Arthritis Res Ther, 2020,22(275).

Jun JI, Lau LF. The Matricellular Protein CCN1 Induces Fibroblast Senescence and Restricts Fibrosis in Cutaneous Wound Healing[J]. Nature Cell Biol, 2010(12):676-685.

Kim KH, Chen CC, Monzon R, et al. The Matricellular Protein CCN1 Promotes Regression of Liver Fibrosis through Induction of Cellular Senescence in Hepatic Myofibroblasts. Mol[J]. Cell Biol, 2013(33):2078-2090.

Bai T, Chen C-C, Lau LF. The matricellular protein CCN1 activates a pro-inflammatory genetic program in murine macrophages[J]. J. Immunol,2010(184):3223-3232.

Bertheloot D, Latz E, Franklin BS. Necroptosis, pyroptosis and apoptosis: an intricate game of cell death[J]. Cell Mol Immunol, 2021,18(5):1106-1121.

Newton K, Dugger DL, Wickliffe KE, et al. Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis[J]. Science,2014(343):1357-1360.

Tang D, Kang R, Berghe TV, et al. The molecular machinery of regulated cell death[J]. Cell Res,2019(29):347-364.

Coornaert I, Hofmans S, Devisscher L, et al. Novel drug discovery strategies for atherosclerosis that target necrosis and necroptosis[J]. Expert Opin Drug Discov,2018,13(6):477-488.

Royce GH, Brown-Borg HM, Deepa SS. The potential role of necroptosis in inflammation and aging[J]. Geroscience, 2019,41(6):795-811.

Zhang X, Ren Z, Xu W, et al. Necroptosis in atherosclerosis[J]. Clin Chim Acta,2022(534):22-28.

Libby P, Buring JE, Badimon L, et al. Atherosclerosis[J]. Nat Rev Dis Primers,2019,5(1):56.

Hsu PL, Chen JS, Wang CY, et al. Shear-Induced CCN1 Promotes Atheroprone Endothelial Phenotypes and Atherosclerosis[J].

Circulation,2019,139(25):2877-2891.

Kim I, Park CS. Angiotensin II type 1 receptor blocker, Fimasartan, reduces vascular smooth muscle cell senescence by inhibiting the CYR61 signaling pathway[J]. Korean Circ J, 2019,49(7):615-626.

Grote K, Bavendiek U, Grothusen C, et al. Stretch-inducibleexpression of the angiogenic factor CCN1 in vascular smooth muscle cells is mediated by Egr-1[J]. J. Biol. Chem,2004(279):55675-55681.

Lee HY, Chung JW, Youn SW, et al. Forkhead transcription factor FOXO3a is a negative regulator of angiogenic immediate early gene CYR61, leading to inhibition of vascular smooth muscle cell proliferation and neointimal hyperplasia[J]. Circ Res,

(100):372-380.

Matsumae H, Yoshida Y, Ono K, et al. CCN1 knockdown suppresses neointimal hyperplasia in a rat artery balloon injury mode[J]. Arterioscler Thromb Vasc Biol,2008(28):1077-1083.

Klingenberg R, Aghlmandi S, Liebetrau C, et al. Cysteine-rich angiogenic inducer 61 (Cyr61): A novel soluble biomarker of acute myocardial injury improves risk stratification after acute coronary syndromes[J]. Eur Heart J,2017(38):3493-3502.

Liu C, Cao Y, He X, et al. Association of Cyr61-cysteine-rich protein 61 and short-term mortality in patients with acute heart failure and coronary heart disease[J]. Biomark Med, 2019(13):1589-1597.

Deng J, Qian X, Li J, et al. Evaluation of serum cysteine-rich protein 61 levels in patients with coronary artery disease[J]. Biomark Med,2018,12(4):329-339.

Szmitko PE, Wang CH, Weisel RD, et al. New markers of inflammation and endothelial cell activation: Part I[J]. Circulation,

(108):1917-1923.

Zhao JF, Chen HY, Wei J, et al. CCN family member 1 deregulates cholesterol metabolism and aggravates atherosclerosis[J]. Acta Physiol (Oxf),2019(225):3209.

Zietzer A, Niepmann ST, Nickenig G, et al. CCN1 regulates cholesterol metabolism-OxLDL enters the matrix[J]. Acta Physiol (Oxf),2019,225(3):3239.

Li W, Li Y, Zhi W, et al. Diagnostic value of using exosome-derived cysteine-rich protein 61 as biomarkers for acute coronary syndrome[J]. Exp Ther Med,2021,22(6):1437.

Tembhre MK, Sriwastva MK, Hote MP, et al. Interleukin-33 Induces Neutrophil Extracellular Trap (NET) Formation and Macrophage Necroptosis via Enhancing Oxidative Stress and Secretion of Proatherogenic Factors in Advanced Atherosclerosis[J]. Antioxidants (Basel),2022,11(12):2343.

Feng N, Anderson M E. CaMKII is a nodal signal for multiple programmed cell death pathways in heart[J]. J. Mol. Cell Cardiol,2017(103):102-109.

Lin J, Li H, Yang M, et al. A role of RIP3-mediated macrophage necrosis in atherosclerosis development[J]. Cell Rep,

(3):200-210.

Liu J, Wu P, Wang Y, et al. Ad-HGF improves the cardiac remodeling of rat following myocardial infarction by upregulating autophagy and necroptosis and inhibiting apoptosis[J]. Am J Transl Res, 2016,8(11):4605-4627.

Gupta K, Phan N, Wang Q, et al. Necroptosis in cardiovascular disease - a new therapeutic target[J]. J Mol Cell Cardiol, 2018(118):26-35.

Papetta A, Gakiopoulou H, Agapitos E, et al. Correlations between CCN1 immunoexpression and myocardial histologic lesions in sudden cardiac death[J]. Am J Forensic Med Pathol, 2013,34(2):169-76.

Roland Klingenberg, Soheila Aghlmandi, Lorenz Räber , et al.

Cysteine-Rich Angiogenic Inducer 61 Improves Prognostic Accuracy of GRACE (Global Registry of Acute Coronary Events) 2.0 Risk Score in Patients With Acute Coronary Syndromes[J]. J Am Heart Assoc,2021,10(20).

Mahendiran T, Klingenberg R, Nanchen D, et al. CCN family member 1 (CCN1) is an early marker of infarct size and left ventricular dysfunction in STEMI patients[J]. Atherosclerosis, 2021(335):77-83.

Hu XM, Chen X, Pang HY, et al. Plasma levels of receptor interacting protein kinase-3 correlated with coronary artery disease[J]. Chin Med J (Engl), 2019,132(12):1400-1405.

Kashlov JK, Donev IS, Doneva JG, et al. Serum levels of RIPK3 and troponin I as potential biomarkers for predicting impaired left ventricular function in patients with myocardial infarction with ST segment elevation and normal troponin I levels prior percutaneous coronary intervention[J]. Biosci Trends, 2016,10(4):294-299.

DOI: http://dx.doi.org/10.12345/yzlcyxzz.v6i2.12356