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652                      学报   Journal of China Pharmaceutical University 2025, 56(5): 645 − 653  第 56 卷

               挥重要作用,不仅是          CVDs 的致病因素,也是潜在               [16]   Wang  PC,  Konja  D,  Singh  S,  et  al.  Endothelial  senescence:
               的治疗靶点。未来的研究和治疗策略有望通过靶                                 from  macro-  to  micro-vasculature and  its  implications  on   car-
                                                                     diovascular health[J]. Int J Mol Sci, 2024, 25(4): 1978.
               向  ECs 衰老,改善血管功能障碍,延缓              CVDs 的发       [17]   Suda M, Paul KH, Minamino T, et al. Senescent cells: a thera-
               展,改善其预后。中药在            ECs 衰老的过程中展现出                  peutic  target  in  cardiovascular  diseases[J].  Cells,  2023,  12(9):
               全方位,多靶点、多机制的优势,为中医药治疗衰老                               1296.
                                                                [18]   Li H, Yang Z, Liang W, et al. DHCR24 insufficiency promotes
               提供新方法与新思路。                                            vascular endothelial  cell  senescence  and  endothelial   dysfunc-
                                                                     tion via inhibition of caveolin-1/ERK signaling[J]. J Gerontol A
                                                                     Biol Sci Med Sci, 2024, 79(4): glae059.
               References
                                                                [19]   Li J, Zhang J, Yu PC, et al. ROS-responsive & scavenging NO
               [1]   López-Otín C, Blasco MA, Partridge L, et al. Hallmarks of ag-  nanomedicine for vascular diseases treatment by inhibiting en-
                    ing: an expanding universe[J]. Cell, 2023, 186(2): 243-278.  doplasmic reticulum stress and improving NO bioavailability[J].
               [2]   Chmielewski PP, Data K, Strzelec B, et al. Human aging and  Bioact Mater, 2024, 37: 239-252.
                    age-related  diseases:  from  underlying  mechanisms  to  pro-  [20]   Aguilar VM, Paul A, Lazarko D, et al. Paradigms of endothe-
                    longevity interventions[J]. Aging Dis, 2024, 16(4): 1853-1877.  lial  stiffening  in  cardiovascular  disease  and  vascular  aging[J].
               [3]   Hayflick  L,  Moorhead  PS.  The  serial  cultivation  of  human  Front Physiol, 2023, 13: 1081119.
                    diploid cell strains[J]. Exp Cell Res, 1961, 25: 585-621.  [21]   Wang XW, Guo ZK, Ding ZF, et al. Endothelin-1 upregulation
               [4]   Zhang  L,  Pitcher  LE,  Yousefzadeh  MJ,  et  al.  Cellular  senes-  mediates aging-related cardiac fibrosis[J]. J Mol Cell Cardiol,
                    cence: a key therapeutic target in aging and diseases[J]. J Clin  2015, 80: 101-109.
                    Invest, 2022, 132(15): e158450.             [22]   Xu  SW,  Ilyas  I,  Little  PJ,  et  al.  Endothelial  dysfunction  in
               [5]   Augustin  HG,  Koh  GY.  A systems  view  of  the  vascular   en-  atherosclerotic cardiovascular diseases and beyond: from mech-
                    dothelium in health and disease[J]. Cell, 2024, 187(18): 4833-  anism  to  pharmacotherapies[J].  Pharmacol  Rev,  2021,  73(3):
                    4858.                                            924-967.
               [6]   Bloom  SI,  Islam  MT,  Lesniewski  LA,  et  al.  Mechanisms  and  [23]   Bu LL, Yuan HH, Xie LL, et al. New dawn for atherosclerosis:
                    consequences of endothelial cell senescence[J]. Nat Rev Cardi-  vascular endothelial cell senescence and death[J]. Int J Mol Sci,
                    ol, 2023, 20(1): 38-51.                          2023, 24(20): 15160.
               [7]   Bloom  SI,  Liu  Y,  Tucker  JR,  et  al.  Endothelial  cell  telomere  [24]   Bian WH, Jing XH, Yang ZY, et al. Downregulation of LncR-
                    dysfunction  induces  senescence  and  results  in  vascular  and  NA  NORAD  promotes  Ox-LDL-induced  vascular  endothelial
                    metabolic impairments[J]. Aging Cell, 2023, 22(8): e13875.  cell  injury  and  atherosclerosis[J].  Aging  (Albany  NY),  2020,
               [8]   Ferrari  S,  Pesce  M.  Stiffness and  aging  in  cardiovascular   dis-  12(7): 6385-6400.
                    eases:  the  dangerous  relationship  between  force  and  [25]   Huang X, Zhou Y, Guo YK, et al. Selenium-doped copper for-
                    senescence[J]. Int J Mol Sci, 2021, 22(7): 3404.  mate nanozymes with antisenescence and oxidative stress reduc-
               [9]   Ya  JY,  Whitby  A,  Bayraktutan  U.  Metabolites  and  metabolic  tion  for  atherosclerosis  treatment[J].  Nano  Lett,  2025,  25(7):
                    functional changes-potential markers for endothelial cell senes-  2662-2669.
                    cence[J]. Biomolecules, 2024, 14(11): 1476.  [26]   Liu MM, Wang DN, Qi CY, et al. Brain ischemia causes sys-
               [10]   Stabenow  LK,  Zibrova  D,  Ender  C,  et  al.  Oxidative  glucose  temic Notch1 activity in endothelial cells to drive atherosclero-
                    metabolism  promotes  senescence  in  vascular  endothelial  sis[J]. Immunity, 2024, 57(9): 2157-2172. e7.
                    cells[J]. Cells, 2022, 11(14): 2213.        [27]   Clayton ZS, Rossman MJ, Mahoney SA, et al. Cellular senes-
               [11]   Wiley CD, Campisi J. The metabolic roots of senescence: mech-  cence contributes to large elastic artery stiffening and endothe-
                    anisms and opportunities for intervention[J]. Nat Metab, 2021,  lial dysfunction  with  aging:  amelioration  with  senolytic   treat-
                    3(10): 1290-1301.                                ment[J]. Hypertension, 2023, 80(10): 2072-2087.
               [12]   Song XX, Yang BY, Qiu FY, et al. High glucose and free fatty  [28]   Xiang QY, Tian F, Xu J, et al. New insight into dyslipidemia-
                    acids  induce  endothelial  progenitor  cell  senescence  via  PGC-  induced  cellular  senescence  in  atherosclerosis[J].  Biol  Rev
                    1α/SIRT1  signaling  pathway[J].  Cell  Biol  Int,  2017,  41(10):  Camb Philos Soc, 2022, 97(5): 1844-1867.
                    1146-1159.                                  [29]   Russo I, Frangogiannis NG. Diabetes-associated cardiac fibro-
               [13]   Hwang  HJ,  Kim  N,  Herman  AB,  et  al.  Factors  and  pathways  sis:  cellular  effectors,  molecular  mechanisms  and  therapeutic
                    modulating endothelial cell senescence in vascular aging[J]. Int  opportunities[J]. J Mol Cell Cardiol, 2016, 90: 84-93.
                    J Mol Sci, 2022, 23(17): 10135.             [30]   Tang XQ, Li PH, Chen HZ. Cardiomyocyte senescence and cel-
               [14]   Chen  MS,  Lee  RT,  Garbern  JC.  Senescence  mechanisms  and  lular communications within myocardial microenvironments[J].
                    targets  in  the  heart[J].  Cardiovasc  Res,  2022,  118(5):  1173-  Front Endocrinol (Lausanne), 2020, 11: 280.
                    1187.                                       [31]   Luan  Y,  Zhu  XF,  Jiao  YX,  et  al.  Cardiac  cell  senescence:
               [15]   Vakka A, Warren JS, Drosatos K. Cardiovascular aging: from  molecular mechanisms, key proteins and therapeutic targets[J].
                    cellular and molecular changes to therapeutic interventions[J]. J  Cell Death Discov, 2024, 10(1): 78.
                    Cardiovasc Aging, 2023, 3(3): 23.           [32]   Qian M, Li S, Xi K, et al. ECM-engineered electrospun fibers
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