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On-line Access: 2024-08-27
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Multiple characteristic alterations and available therapeutic strategies of cellular senescence
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Abstract: Given its state of stable proliferative inhibition, cellular senescence is primarily depicted as a critical mechanism by which organisms delay the progression of carcinogenesis. Cells undergoing senescence are often associated with the alteration of a series of specific features and functions, such as metabolic shifts, stemness induction, and microenvironment remodeling. However, recent research has revealed more complexity associated with senescence, including adverse effects on both physiological and pathological processes. How organisms evade these harmful consequences and survive has become an urgent research issue. Several therapeutic strategies targeting senescence, including senolytics, senomorphics, immunotherapy, and function restoration, have achieved initial success in certain scenarios. In this review, we describe in detail the characteristic changes associated with cellular senescence and summarize currently available countermeasures.
[1]AirdKM, ZhangG, LiH, et al., 2013. Suppression of nucleotide metabolism underlies the establishment and maintenance of oncogene-induced senescence. Cell Rep, 3(4):1252-1265.
[2]AlspachE, FlanaganKC, LuoXM, et al., 2014. p38MAPK plays a crucial role in stromal-mediated tumorigenesis. Cancer Discov, 4(6):716-729.
[3]AmorC, FeuchtJ, LeiboldJ, et al., 2020. Senolytic CAR T cells reverse senescence-associated pathologies. Nature, 583(7814):127-132.
[4]AroraS, ThompsonPJ, WangY, et al., 2021. Invariant natural killer T cells coordinate removal of senescent cells. Med (N Y), 2(8):938-950.
[5]BaarMP, BrandtRMC, PutavetDA, et al., 2017. Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell, 169(1):132-147.e16.
[6]BaiZS, PengYL, YeXY, et al., 2022. Autophagy and cancer treatment: four functional forms of autophagy and their therapeutic applications. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 23(2):89-101.
[7]BatlleE, CleversH, 2017. Cancer stem cells revisited. Nat Med, 23(10):1124-1134.
[8]bin ImtiazMK, JaegerBN, BottesS, et al., 2021. Declining lamin B1 expression mediates age-dependent decreases of hippocampal stem cell activity. Cell Stem Cell, 28(5):967-977.e8.
[9]BloklandKEC, PouwelsSD, SchuligaM, et al., 2020. Regulation of cellular senescence by extracellular matrix during chronic fibrotic diseases. Clin Sci (Lond), 134(20):2681-2706.
[10]CarlstenM, ChildsRW, 2015. Genetic manipulation of NK cells for cancer immunotherapy: techniques and clinical implications. Front Immunol, 6:266.
[11]ChaleckisR, MurakamiI, TakadaJ, et al., 2016. Individual variability in human blood metabolites identifies age-related differences. Proc Natl Acad Sci USA, 113(16):4252-4259.
[12]ChambersCR, RitchieS, PereiraBA, et al., 2021. Overcoming the senescence-associated secretory phenotype (SASP): a complex mechanism of resistance in the treatment of cancer. Mol Oncol, 15(12):3242-3255.
[13]ChenF, LongQL, FuD, et al., 2018. Targeting SPINK1 in the damaged tumour microenvironment alleviates therapeutic resistance. Nat Commun, 9:4315.
[14]ChengH, XuanHW, GreenCD, et al., 2018. Repression of human and mouse brain inflammaging transcriptome by broad gene-body histone hyperacetylation. Proc Natl Acad Sci USA, 115(29):7611-7616.
[15]ChengT, RodriguesN, ShenH, et al., 2000. Hematopoietic stem cell quiescence maintained by p21cip1/waf1. Science, 287(5459):1804-1808.
[16]ChienY, ScuoppoC, WangXW, et al., 2011. Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. Genes Dev, 25(20):2125-2136.
[17]ContrepoisK, CoudereauC, BenayounBA, et al., 2017. Histone variant H2A.J accumulates in senescent cells and promotes inflammatory gene expression. Nat Commun, 8:14995.
[18]CrespoJ, SunHY, WellingTH, et al., 2013. T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment. Curr Opin Immunol, 25(2):214-221.
[19]CrosbyCM, KronenbergM, 2018. Tissue-specific functions of invariant natural killer T cells. Nat Rev Immunol, 18(9):559-574.
[20]CruickshanksHA, McbryanT, NelsonDM, et al., 2013. Senescent cells harbour features of the cancer epigenome. Nat Cell Biol, 15(12):1495-1506.
[21]del Gaizo MooreV, BrownJR, CertoM, et al., 2007. Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737. J Clin Invest, 117(1):112-121.
[22]DelfarahA, ParrishS, JungeJA, et al., 2019. Inhibition of nucleotide synthesis promotes replicative senescence of human mammary epithelial cells. J Biol Chem, 294(27):10564-10578.
[23]di MitriD, AlimontiA, 2016. Non-cell-autonomous regulation of cellular senescence in cancer. Trends Cell Biol, 26(3):215-226.
[24]DörrJR, YuY, MilanovicM, et al., 2013. Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. Nature, 501(7467):421-425.
[25]EckerBL, KaurA, DouglassSM, et al., 2019. Age-related changes in HAPLN1 increase lymphatic permeability and affect routes of melanoma metastasis. Cancer Discov, 9(1):82-95.
[26]ErbeR, WangZY, WuS, et al., 2021. Evaluating the impact of age on immune checkpoint therapy biomarkers. Cell Rep, 36(8):109599.
[27]FagetDV, RenQH, StewartSA, 2019. Unmasking senescence: context-dependent effects of SASP in cancer. Nat Rev Cancer, 19(8):439-453.
[28]FeinsS, KongWM, WilliamsEF, et al., 2019. An introduction to chimeric antigen receptor (CAR) T-cell immunotherapy for human cancer. Am J Hematol, 94(S1):S3-S9.
[29]Fuhrmann-StroissniggH, LingYY, ZhaoJ, et al., 2017. Identification of HSP90 inhibitors as a novel class of senolytics. Nat Commun, 8:422.
[30]GanKJ, SüdhofTC, 2019. Specific factors in blood from young but not old mice directly promote synapse formation and NMDA-receptor recruitment. Proc Natl Acad Sci USA, 116(25):12524-12533.
[31]García-PratL, Martínez-VicenteM, PerdigueroE, et al., 2016. Autophagy maintains stemness by preventing senescence. Nature, 529(7584):37-42.
[32]GomesAP, IlterD, LowV, et al., 2020. Age-induced accumulation of methylmalonic acid promotes tumour progression. Nature, 585(7824):283-287.
[33]GrosseL, WagnerN, EmelyanovA, et al., 2020. Defined p16High senescent cell types are indispensable for mouse healthspan. Cell Metab, 32(1):87-99.e6.
[34]GuerreroA, HerranzN, SunB, et al., 2019. Cardiac glycosides are broad-spectrum senolytics. Nat Metab, 1(11):1074-1088.
[35]HanL, LongQL, LiSJ, et al., 2020. Senescent stromal cells promote cancer resistance through SIRT1 loss-potentiated overproduction of small extracellular vesicles. Cancer Res, 80(16):3383-3398.
[36]HaynesL, EatonSM, BurnsEM, et al., 2003. CD4 T cell memory derived from young naive cells functions well into old age, but memory generated from aged naive cells functions poorly. Proc Natl Acad Sci USA, 100(25):15053-15058.
[37]HensonSM, LannaA, RiddellNE, et al., 2014. p38 signaling inhibits MTORC1-independent autophagy in senescent human CD8+ T cells. J Clin Invest, 124(9):4004-4016.
[38]Hernandez-SeguraA, NehmeJ, DemariaM, 2018. Hallmarks of cellular senescence. Trends Cell Biol, 28(6):436-453.
[39]HerranzN, GallageS, MelloneM, et al., 2015. mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype. Nat Cell Biol, 17(9):1205-1217.
[40]HoTT, WarrMR, AdelmanER, et al., 2017. Autophagy maintains the metabolism and function of young and old stem cells. Nature, 543(7644):205-210.
[41]HongMH, ClubbJD, ChenYY, 2020. Engineering CAR-T cells for next-generation cancer therapy. Cancer Cell, 38(4):473-488.
[42]HwangHJ, LeeYR, KangD, et al., 2020. Endothelial cells under therapy-induced senescence secrete CXCL11, which increases aggressiveness of breast cancer cells. Cancer Lett, 490:100-110.
[43]JengMY, HullPA, FeiMJ, et al., 2018. Metabolic reprogramming of human CD8+ memory T cells through loss of SIRT1. J Exp Med, 215(1):51-62.
[44]JeonOH, KimC, LabergeRM, et al., 2017. Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment. Nat Med, 23(6):775-781.
[45]JinWN, ShiKB, HeWY, et al., 2021. Neuroblast senescence in the aged brain augments natural killer cell cytotoxicity leading to impaired neurogenesis and cognition. Nat Neurosci, 24(1):61-73.
[46]JohmuraY, YamanakaT, OmoriS, et al., 2021. Senolysis by glutaminolysis inhibition ameliorates various age-associated disorders. Science, 371(6526):265-270.
[47]KalamakisG, BrüneD, RavichandranS, et al., 2019. Quiescence modulates stem cell maintenance and regenerative capacity in the aging brain. Cell, 176(6):1407-1419.e14.
[48]KaleA, SharmaA, StolzingA, et al., 2020. Role of immune cells in the removal of deleterious senescent cells. Immun Ageing, 17:16.
[49]KaplonJ, ZhengL, MeisslK, et al., 2013. A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence. Nature, 498(7452):109-112.
[50]KaurA, WebsterMR, MarchbankK, et al., 2016. sFRP2 in the aged microenvironment drives melanoma metastasis and therapy resistance. Nature, 532(7598):250-254.
[51]KaurA, EckerBL, DouglassSM, et al., 2019. Remodeling of the collagen matrix in aging skin promotes melanoma metastasis and affects immune cell motility. Cancer Discov, 9(1):64-81.
[52]KirklandJL, TchkoniaT, 2020. Senolytic drugs: from discovery to translation. J Intern Med, 288(5):518-536.
[53]KowaldA, PassosJF, KirkwoodTBL, 2020. On the evolution of cellular senescence. Aging Cell, 19(12):e13270.
[54]KrtolicaA, ParrinelloS, LockettS, et al., 2001. Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging. Proc Natl Acad Sci USA, 98(21):12072-12077.
[55]KuilmanT, MichaloglouC, VredeveldLCW, et al., 2008. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell, 133(6):1019-1031.
[56]KuilmanT, MichaloglouC, MooiWJ, et al., 2010. The essence of senescence. Genes Dev, 24(22):2463-2479.
[57]LawrensonK, GrunB, BenjaminE, et al., 2010. Senescent fibroblasts promote neoplastic transformation of partially transformed ovarian epithelial cells in a three-dimensional model of early stage ovarian cancer. Neoplasia, 12(4):317-325.
[58]LeeS, SchmittCA, 2019. The dynamic nature of senescence in cancer. Nate Cell Biol, 21(1):94-101.
[59]LeeS, YuY, TrimpertJ, et al., 2021. Virus-induced senescence is a driver and therapeutic target in COVID-19. Nature, 599(7884):283-289.
[60]LeiQ, GaoF, LiuT, et al., 2021. Extracellular vesicles deposit PCNA to rejuvenate aged bone marrow-derived mesenchymal stem cells and slow age-related degeneration. Sci Transl Med, 13(578):eaaz8697.
[61]LeviN, PapismadovN, SolomonovI, et al., 2020. The ECM path of senescence in aging: components and modifiers. FEBS J, 287(13):2636-2646.
[62]L'HôteV, CourbeyretteR, PinnaG, et al., 2021. Ouabain and chloroquine trigger senolysis of BRAF-V600E-induced senescent cells by targeting autophagy. Aging Cell, 20(9):e13447.
[63]LiFM, HuangyangP, BurrowsM, et al., 2020. FBP1 loss disrupts liver metabolism and promotes tumorigenesis through a hepatic stellate cell senescence secretome. Nat Cell Biol, 22(6):728-739.
[64]LiH, LakshmikanthT, GarofaloC, et al., 2011. Pharmacological activation of p53 triggers anticancer innate immune response through induction of ULBP2. Cell Cycle, 10(19):3346-3358.
[65]LianJY, YueY, YuWN, et al., 2020. Immunosenescence: a key player in cancer development. J Hematol Oncol, 13:151.
[66]LiuY, ElfSE, MiyataY, et al., 2009. p53 regulates hematopoietic stem cell quiescence. Cell Stem Cell, 4(1):37-48.
[67]LiuZY, LeungD, ThrushK, et al., 2020. Underlying features of epigenetic aging clocks in vivo and in vitro. Aging Cell, 19(10):e13229.
[68]LizardoDY, LinYL, GokcumenO, et al., 2017. Regulation of lipids is central to replicative senescence. Mol BioSyst, 13(3):498-509.
[69]LooTM, MiyataK, TanakaY, et al., 2020. Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer. Cancer Sci, 111(2):304-311.
[70]LujambioA, AkkariL, SimonJ, et al., 2013. Non-cell-autonomous tumor suppression by p53. Cell, 153(2):449-460.
[71]ManfrediR, 2004. HIV infection and advanced age: emerging epidemiological, clinical, and management issues. Ageing Res Rev, 3(1):31-54.
[72]MavrogonatouE, PratsinisH, PapadopoulouA, et al., 2019. Extracellular matrix alterations in senescent cells and their significance in tissue homeostasis. Matrix Biol, 75-76:27-42.
[73]MeyersAK, ZhuXW, 2020. The NLRP3 inflammasome: metab
[74]olic regulation and contribution to inflammaging. Cells, 9(8):1808.
[75]MilanovicM, FanDNY, BelenkiD, et al., 2018a. Senescence-associated reprogramming promotes cancer stemness. Nature, 553(7686):96-100.
[76]MilanovicM, YuY, SchmittCA, 2018b. The senescence-stemness alliance‒a cancer-hijacked regeneration principle. Trends Cell Biol, 28(12):1049-1061.
[77]MinhasPS, Latif-HernandezA, McreynoldsMR, et al., 2021. Restoring metabolism of myeloid cells reverses cognitive decline in ageing. Nature, 590(7844):122-128.
[78]MontesCL, ChapovalAI, NelsonJ, et al., 2008. Tumor-induced senescent T cells with suppressor function: a potential form of tumor immune evasion. Cancer Res, 68(3):870-879.
[79]MoyonS, FrawleyR, MarechalD, et al., 2021. TET1-mediated DNA hydroxymethylation regulates adult remyelination in mice. Nat Commun, 12:3359.
[80]Muñoz-GalvánS, Lucena-CacaceA, PerezM, et al., 2019. Tumor cell-secreted PLD increases tumor stemness by senescence-mediated communication with microenvironment. Oncogene, 38(8):1309-1323.
[81]NacarelliT, FukumotoT, ZundellJA, et al., 2020. NAMPT inhibition suppresses cancer stem-like cells associated with therapy-induced senescence in ovarian cancer. Cancer Res, 80(4):890-900.
[82]OltraSS, Peña-ChiletM, FlowerK, et al., 2019. Acceleration in the DNA methylation age in breast cancer tumours from very young women. Sci Rep, 9(1):14991.
[83]Otero-AlbiolD, CarneroA, 2021. Cellular senescence or stemness: hypoxia flips the coin. J Exp Clin Cancer Res, 40:243.
[84]OzsvariB, NuttallJR, SotgiaF, et al., 2018. Azithromycin and roxithromycin define a new family of “senolytic” drugs that target senescent human fibroblasts. Aging, 10(11):3294-3307.
[85]PathanM, FonsekaP, ChittiSV, et al., 2019. Vesiclepedia 2019: a compendium of RNA, proteins, lipids and metabolites in extracellular vesicles. Nucleic Acids Res, 47(D1):D516-D519.
[86]PawelecG, 2019. Does patient age influence anti-cancer immunity? Semin Immunopathol, 41(1):125-131.
[87]PazolliE, AlspachE, MilczarekA, et al., 2012. Chromatin remodeling underlies the senescence-associated secretory phenotype of tumor stromal fibroblasts that supports cancer progression. Cancer Res, 72(9):2251-2261.
[88]PereiraBI, DevineOP, Vukmanovic-StejicM, et al., 2019. Senescent cells evade immune clearance via HLA-E-mediated NK and CD8+ T cell inhibition. Nat Commun, 10:2387.
[89]PerriguePM, RakoczyM, PawlickaKP, et al., 2020. Cancer stem cell-inducing media activates senescence reprogramming in fibroblasts. Cancers, 12(7):1745.
[90]PoblockaM, BasseyAL, SmithVM, et al., 2021. Targeted clearance of senescent cells using an antibody-drug conjugate against a specific membrane marker. Sci Rep, 11:20358.
[91]QingYJ, LiH, ZhaoYZ, et al., 2021. One-two punch ther
[92]apy for the treatment of T-cell malignancies involving p53-dependent cellular senescence. Oxid Med Cell Longev, 2021:5529518.
[93]RajendranP, AlzahraniAM, HaniehHN, et al., 2019. Autophagy and senescence: a new insight in selected human diseases. J Cell Physiol, 234(12):21485-21492.
[94]RezvaniK, RouceR, LiuEL, et al., 2017. Engineering natural killer cells for cancer immunotherapy. Mol Ther, 25(8):1769-1781.
[95]RitschkaB, StorerM, MasA, et al., 2017. The senescence-associated secretory phenotype induces cellular plasticity and tissue regeneration. Genes Dev, 31(2):172-183.
[96]RuggeriL, CapanniM, UrbaniE, et al., 2002. Effectiveness of donor natural killer cell alloreactivity in mismatched hematopoietic transplants. Science, 295(5562):2097-2100.
[97]SahuA, MamiyaH, ShindeSN, et al., 2018. Age-related declines in α-Klotho drive progenitor cell mitochondrial dysfunction and impaired muscle regeneration. Nat Commun, 9:4859.
[98]SalazarG, CullenA, HuangJW, et al., 2020. SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence. Autophagy, 16(6):1092-1110.
[99]SchaferMJ, WhiteTA, IijimaK, et al., 2017. Cellular senescence mediates fibrotic pulmonary disease. Nat Commun, 8:14532.
[100]SchmittCA, 2018. UnSASPing senescence: unmasking tumor suppression? Cancer Cell, 34(1):6-8.
[101]SebastianT, MalikR, ThomasS, et al., 2005. C/EBPβ cooperates with RB:E2F to implement RasV12-induced cellular senescence. EMBO J, 24(18):3301-3312.
[102]SegelM, NeumannB, HillMFE, et al., 2019. Niche stiffness underlies the ageing of central nervous system progenitor cells. Nature, 573(7772):130-134.
[103]SerranoM, 2017. Ageing: tools to eliminate senescent cells. Nature, 545(7654):294-295.
[104]ShahY, VermaA, MardersteinAR, et al., 2021. Pan-cancer analysis reveals molecular patterns associated with age. Cell Rep, 37(10):110100.
[105]SharmaA, AlmasanA, 2021. Autophagy and PTEN in DNA damage-induced senescence. Adv Cancer Res, 150:249-284.
[106]ShiHZ, ZengJC, ShiSH, et al., 2021. Extracellular vesicles of GMSCs alleviate aging-related cell senescence. J Dent Res, 100(3):283-292.
[107]StorerM, MasA, Robert-MorenoA, et al., 2013. Senescence is a developmental mechanism that contributes to embryonic growth and patterning. Cell, 155(5):1119-1130.
[108]SturmlechnerI, ZhangC, SineCC, et al., 2021. p21 produces a bioactive secretome that places stressed cells under immunosurveillance. Science, 374(6567):eabb3420.
[109]SudaM, ShimizuI, KatsuumiG, et al., 2021. Senolytic vaccination improves normal and pathological age-related phenotypes and increases lifespan in progeroid mice. Nat Aging, 1(12):1117-1126.
[110]SugrueVJ, ZollerJA, NarayanP, et al., 2021. Castration delays epigenetic aging and feminizes DNA methylation at androgen-regulated loci. eLife, 10:e64932.
[111]TakahashiA, OkadaR, NagaoK, et al., 2017. Exosomes maintain cellular homeostasis by excreting harmful DNA from cells. Nat Commun, 8:15287.
[112]ThompsonPJ, ShahA, NtranosV, et al., 2019. Targeted elimination of senescent beta cells prevents type 1 diabetes. Cell Metab, 29(5):1045-1060.e10.
[113]TosoA, RevandkarA, di MitriD, et al., 2014. Enhancing chemotherapy efficacy in Pten-deficient prostate tumors by activating the senescence-associated antitumor immunity. Cell Rep, 9(1):75-89.
[114]van NielG, D'AngeloG, RaposoG, 2018. Shedding light on the cell biology of extracellular vesicles. Nat Rev Mol Cell Biol, 19(4):213-228.
[115]VenkeiZG, YamashitaYM, 2018. Emerging mechanisms of asymmetric stem cell division. J Cell Biol, 217(11):3785-3795.
[116]WangC, VegnaS, JinHJ, et al., 2019. Inducing and exploiting vulnerabilities for the treatment of liver cancer. Nature, 574(7777):268-272.
[117]WangRW, ViganòS, Ben-DavidU, et al., 2021. Aneuploid senescent cells activate NF-κB to promote their immune clearance by NK cells. EMBO Rep, 22(8):e52032.
[118]WeberR, GrothC, LasserS, et al., 2021. IL-6 as a major regulator of MDSC activity and possible target for cancer immunotherapy. Cell Immunol, 359:104254.
[119]WileyCD, CampisiJ, 2021. The metabolic roots of senescence: mechanisms and opportunities for intervention. Nat Metab, 3(10):1290-1301.
[120]XuQX, LongQL, ZhuDX, et al., 2019. Targeting amphiregulin (AREG) derived from senescent stromal cells diminishes cancer resistance and averts programmed cell death 1 ligand (PD-L1)-mediated immunosuppression. Aging Cell, 18(6):e13027.
[121]XueW, ZenderL, MiethingC, et al., 2007. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature, 445(7128):656-660.
[122]YagerEJ, AhmedM, LanzerK, et al., 2008. Age-associated decline in T cell repertoire diversity leads to holes in the repertoire and impaired immunity to influenza virus. J Exp Med, 205(3):711-723.
[123]YosefR, PilpelN, Tokarsky-AmielR, et al., 2016. Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL. Nat Commun, 7:11190.
[124]YoshidaS, NakagamiH, HayashiH, et al., 2020. The CD153 vaccine is a senotherapeutic option for preventing the accumulation of senescent T cells in mice. Nat Commun, 11:2482.
[125]ZhangBY, FuD, XuQX, et al., 2018. The senescence-associated secretory phenotype is potentiated by feedforward regulatory mechanisms involving Zscan4 and TAK1. Nat Commun, 9:1723.
[126]ZhuHY, LiQQ, LiaoTP, et al., 2021. Metabolomic profiling of single enlarged lysosomes. Nat Methods, 18(7):788-798.
[127]ZhuY, TchkoniaT, PirtskhalavaT, et al., 2015. The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell, 14(4):644-658.
[128]ZhuY, TchkoniaT, Fuhrmann-StroissniggH, et al., 2016. Identification of a novel senolytic agent, navitoclax, targeting the Bcl-2 family of anti-apoptotic factors. Aging Cell, 15(3):428-435.
Yunzi ZHAO, Hui LI, Qinglong GUO, Hui HUI. Multiple characteristic alterations and available therapeutic strategies of cellular senescence[J]. Journal of Zhejiang University Science B, 2023, 24(2): 101-114.
@article{title="Multiple characteristic alterations and available therapeutic strategies of cellular senescence",
author="Yunzi ZHAO, Hui LI, Qinglong GUO, Hui HUI",
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publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2200178"
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