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第41卷第10期
               ·1562 ·                           南 京    医 科 大 学 学         报                        2021年10月


              CTRP12 和 CTRP13 具有抗炎和抗动脉粥样硬化作                          sclerosis,2018,278:197-209
              用。CTRP 家庭成员通过调节糖脂代谢影响内皮细                          [9] APPARI M,BREITBART A,BRANDES F,et al. C1q ⁃
                                                                     TNF⁃related protein⁃9 promotes cardiac hypertrophy and
              胞炎症和斑块血管形成。CTRP1、CTRP3 和 CTRP9
              抑制内膜增生和血管平滑肌细胞增殖,对缺血心肌                                 failure[J]. Circ Res,2017,120(1):66-77
                                                                [10] ZHANG P,HUANG C,LI J,et al. Globular CTRP9 inhib⁃
              有保护作用。CTRP1 和 CTRP5 在 CAD 患者中升
                                                                     its oxLDL⁃induced inflammatory response in RAW 264.7
              高。相反,CTRP3、CTRP9、CTRP12 和 CTRP13 作为
                                                                     macrophages via AMPK activation[J]. Mol Cell Biochem,
              CAD的保护因子在CAD患者中降低。CTRP大家族
                                                                     2016,417(1⁃2):67-74
              的成员在多个系统都有广泛的功能,本文解读了                             [11] LIU Q,ZHANG H,LIN J,et al. C1q/TNF⁃related protein
              CTRP 家族在 CAD 发生及发展中各个阶段的作用。                            9 inhibits the cholesterol⁃induced vascular smooth muscle
              CTRP家族正不断发展壮大,对于CTRP家族成员的                              cell phenotype switch and cell dysfunction by activating
              深入研究将为今后临床治疗代谢综合征、冠状动脉                                 AMP ⁃ dependent kinase[J]. J Cell Mol Med,2017,21
              疾病提供新的思路。                                             (11):2823-2836
                                                                [12] LI YX,RUN L,SHI T,et al. CTRP9 regulates hypoxia⁃me⁃
             [参考文献]
                                                                     diated human pulmonary artery smooth muscle cell prolif⁃
             [1] MUENDLEIN A,LEIHERER A,SAELY C,et al. The nov⁃      eration,apoptosis and migration via TGF ⁃ beta1/ERK1/2
                   el adipokine CTRP1 is significantly associated with the in⁃  signaling pathway[J]. Biochem Biophys Res Commun,
                   cidence of major adverse cardiovascular events[J]. Ath⁃  2017,490(4):1319-1325
                   erosclerosis,2019,286:1-6                    [13] SUN H,ZHU X,ZHOU Y,et al. C1q/TNF⁃related protein⁃
             [2] YUASA D,OHASHI K,SHIBATA R,et al. C1q/TNF⁃re⁃       9 ameliorates ox ⁃ LDL ⁃ induced endothelial dysfunction
                   lated protein⁃1 functions to protect against acute ischemic  via PGC⁃1alpha/AMPK⁃mediated antioxidant enzyme in⁃
                   injury in the heart[J]. FASEB J,2016,30(3):1065-  duction[J]. Int J Mol Sci,2017,18(6):1097
                   1075                                         [14] ZHANG H,GONG X,NI S,et al. C1q/TNF⁃related protein
             [3] ZHANG Y,LIU C,LIU J,et al. Implications of C1q/TNF⁃  ⁃9 attenuates atherosclerosis through AMPK⁃NLRP3 in⁃
                   related protein superfamily in patients with coronary ar⁃  flammasome singling pathway[J]. Int Immunopharmacol,
                   tery disease[J]. Sci Rep,2020,10(1):878           2019,77:105934
             [4] LIN J,LIU Q,ZHANG H,et al. C1q/Tumor necrosis factor  [15] LIU M,YIN L,LI W,et al. C1q/TNF⁃related protein⁃9
                   ⁃related protein⁃3 protects macrophages against LPS⁃in⁃  promotes macrophage polarization and improves cardiac
                   duced lipid accumulation,inflammation and phenotype  dysfunction after myocardial infarction[J]. J Cell Physiol,
                   transition via PPARgamma and TLR4⁃mediated pathways  2019,234(10):18731-18747
                  [J]. Oncotarget,2017,8(47):82541-82557        [16] LIU T,XU B,LIU Z. CTRP9 alleviates inflammation to
             [5] CHEN L,QIN L,LIU X,et al. CTRP3 Alleviates ox⁃LDL⁃  ameliorate myocardial infarction in rats by activating Nrf2
                   induced inflammatory response and endothelial dysfunc⁃  [J]. Minerva Endocrinol,2020,45(3):268-270
                   tion in mouse aortic endothelial cells by activating the  [17] CHEN J Y,LEI S Y,LI T T,et al. CTRP9 induces iNOS
                   PI3K/Akt/eNOS pathway[J]. Inflammation,2019,42(4):  expression through JAK2/STAT3 pathway in Raw 264.7
                   1350-1359                                         and peritoneal macrophages[J]. Biochem Biophys Res
             [6] 彭中兴,陈昊颖,李琳青,等. C1q肿瘤坏死因子相关蛋                         Commun,2020,523(1):98-104
                   白3对AMI患者外周血中间型(CD14~(++)CD16~+)单             [18] FADAEI R,MORADI N,KAZEMI T,et al. Decreased se⁃
                   核细胞分化的影响及其机制[J]. 东南大学学报(医学                        rum levels of CTRP12/adipolin in patients with coronary
                   版),2019,38(2):242-248                             artery disease in relation to inflammatory cytokines and
             [7] SHEN Y,LI C,ZHANG R Y,et al. Association of in⁃     insulin resistance[J]. Cytokine,2019,113:326-331
                   creased serum CTRP5 levels with in⁃stent restenosis after  [19] WANG C,XU W,LIANG M,et al. CTRP13 inhibits ath⁃
                   coronary drug⁃eluting stent implantation:CTRP5 promot⁃  erosclerosis via autophagy⁃lysosome⁃dependent degrada⁃
                   ing inflammation,migration and proliferation in vascular  tion of CD36[J]. FASEB J,2019,33(2):2290-2300
                   smooth muscle cells[J]. Int J Cardiol,2017,228:129-  [20] XIN Y,ZHANG D,FU Y,et al. C1qTNF⁃related protein 1
                   136                                               improve insulin resistance by reducing phosphorylation of
             [8] LI C,CHEN J W,LIU Z H,et al. CTRP5 promotes trans⁃  serine 1101 in insulin receptor substrate 1[J]. Endocr J,
                  cytosis and oxidative modification of low⁃density lipopro⁃  2017,64(8):787-796
                  tein and the development of atherosclerosis[J]. Athero⁃  [21] YAGMUR E,BUERGERHAUSEN D,KOEK G H,et al.
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