REFERENCES
1. Bhakta N, Liu Q, Yeo F, et al. Cumulative burden of cardiovascular morbidity in paediatric, adolescent, and young adult survivors of Hodgkin’s lymphoma: an analysis from the St Jude lifetime cohort study. The Lancet Oncology 2016;17:1325-34.
2. Iconaru EI, Ciucurel MM, Georgescu L, Ciucurel C. Hand grip strength as a physical biomarker of aging from the perspective of a Fibonacci mathematical modeling. BMC Geriatr 2018;18:296.
3. Huang S, Parekh V, Waisman J, et al. Cutaneous metastasectomy: is there a role in breast cancer? J Surg Oncol 2022; doi: 10.1002/jso.26870.
4. Stec R, Bodnar L, Smoter M, Mączewski M, Szczylik C. Metastatic colorectal cancer in the elderly: an overview of the systemic treatment modalities (Review). Oncol Lett 2011;2:3-11.
5. Syrigos KN, Karachalios D, Karapanagiotou EM, Nutting CM, Manolopoulos L, Harrington KJ. Head and neck cancer in the elderly: an overview on the treatment modalities. Cancer Treat Rev 2009;35:237-45.
6. Cupit-Link MC, Kirkland JL, Ness KK, et al. Biology of premature ageing in survivors of cancer. ESMO Open 2017;2:e000250.
7. Sung H, Ferlay J, Siegel RL, et al. Global cancer statistics 2020: globocan estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 2021;71:209-49.
8. Qin S, Schulte BA, Wang GY. Role of senescence induction in cancer treatment. World J Clin Oncol 2018;9:180-7.
9. Luo H, Yount C, Lang H, et al. Activation of p53 with Nutlin-3a radiosensitizes lung cancer cells via enhancing radiation-induced premature senescence. Lung Cancer 2013;81:167-73.
10. Sherr CJ, Beach D, Shapiro GI. Targeting CDK4 and CDK6: from discovery to therapy. Cancer Discov 2016;6:353-67.
11. Rader J, Russell MR, Hart LS, et al. Dual CDK4/CDK6 inhibition induces cell-cycle arrest and senescence in neuroblastoma. Clin Cancer Res 2013;19:6173-82.
12. Yoshida A, Lee EK, Diehl JA. Induction of therapeutic senescence in vemurafenib-resistant melanoma by extended inhibition of CDK4/6. Cancer Res 2016;76:2990-3002.
13. Klein ME, Dickson MA, Antonescu C, et al. PDLIM7 and CDH18 regulate the turnover of MDM2 during CDK4/6 inhibitor therapy-induced senescence. Oncogene 2018;37:5066-78.
14. Manfredi MG, Ecsedy JA, Meetze KA, et al. Antitumor activity of MLN8054, an orally active small-molecule inhibitor of Aurora A kinase. Proc Natl Acad Sci U S A 2007;104:4106-11.
15. Liu Y, Hawkins OE, Su Y, Vilgelm AE, Sobolik T, Thu YM, et al. Targeting aurora kinases limits tumour growth through DNA damage-mediated senescence and blockade of NF-kappaB impairs this drug-induced senescence. EMBO Mol Med 2013;5:149-66.
16. Liu Y, Hawkins OE, Su Y, et al. Targeting aurora kinases limits tumour growth through DNA damage-mediated senescence and blockade of NF-κB impairs this drug-induced senescence. EMBO Mol Med 2013;5:149-66.
17. Wysong DR, Chakravarty A, Hoar K, Ecsedy JA. The inhibition of Aurora A abrogates the mitotic delay induced by microtubule perturbing agents. Cell Cycle 2009;8:876-88.
18. Dobrzanski MJ, Rewers-Felkins KA, Quinlin IS, et al. Autologous MUC1-specific Th1 effector cell immunotherapy induces differential levels of systemic TReg cell subpopulations that result in increased ovarian cancer patient survival. Clin Immunol 2009;133:333-52.
19. Rosemblit C, Datta J, Lowenfeld L, et al. Oncodriver inhibition and CD4+ Th1 cytokines cooperate through Stat1 activation to induce tumor senescence and apoptosis in HER2+ and triple negative breast cancer: implications for combining immune and targeted therapies. Oncotarget 2018;9:23058-77.
20. Luheshi N, Davies G, Poon E, Wiggins K, McCourt M, Legg J. Th1 cytokines are more effective than Th2 cytokines at licensing anti-tumour functions in CD40-activated human macrophages in vitro. Eur J Immunol 2014;44:162-72.
21. Iconaru EI, Ciucurel C. Hand grip strength variability during serial testing as an entropic biomarker of aging: a Poincaré plot analysis. BMC Geriatr 2020;20:12.
22. Cooper R, Kuh D, Hardy R. Mortality Review Group. Objectively measured physical capability levels and mortality: systematic review and meta-analysis. BMJ 2010;341:c4467.
23. Celis-Morales CA, Welsh P, Lyall DM, et al. Associations of grip strength with cardiovascular, respiratory, and cancer outcomes and all cause mortality: prospective cohort study of half a million UK Biobank participants. BMJ 2018;361:k1651.
24. Uziel O, Lahav M, Shargian L, et al. Premature ageing following allogeneic hematopoietic stem cell transplantation. Bone Marrow Transplant 2020;55:1438-46.
25. Uziel O, Lahav M, Shargian L, et al. Correction: Premature ageing following allogeneic hematopoietic stem cell transplantation. Bone Marrow Transplant 2020;55:1519.
26. Arora M, Sun CL, Ness KK, et al. Physiologic Frailty in nonelderly hematopoietic cell transplantation patients: results from the bone marrow transplant survivor study. JAMA Oncol 2016;2:1277-86.
27. Kim DK, Lee HS, Park JY, et al. Risk of cardiovascular intervention after androgen deprivation therapy in prostate cancer patients with a prior history of ischemic cardiovascular and cerebrovascular disease: a nationwide population-based cohort study. Urol Oncol 2022;40:6.e11-9.
28. Leer P. The risk of cardiovascular disease, fracture, dementia, and cancer after long-term hormone therapy in perimenopausal and postmenopausal women. Am Fam Physician 2018;98:117-8.
29. Aleman BM, Moser EC, Nuver J, et al. Cardiovascular disease after cancer therapy. EJC Suppl 2014;12:18-28.
30. O’Farrell S, Garmo H, Holmberg L, Adolfsson J, Stattin P, Van Hemelrijck M. Risk and timing of cardiovascular disease after androgen-deprivation therapy in men with prostate cancer. J Clin Oncol 2015;33:1243-51.
31. Scott JM, Koelwyn GJ, Hornsby WE, et al. Exercise therapy as treatment for cardiovascular and oncologic disease after a diagnosis of early-stage cancer. Semin Oncol 2013;40:218-28.
32. Lipshultz SE, Landy DC, Lopez-Mitnik G, et al. Cardiovascular status of childhood cancer survivors exposed and unexposed to cardiotoxic therapy. J Clin Oncol 2012;30:1050-7.
33. Hudson MM, Ness KK, Gurney JG, et al. Clinical ascertainment of health outcomes among adults treated for childhood cancer. JAMA 2013;309:2371-81.
34. Robinson PD, Tomlinson D, Beauchemin M, et al. Identifying clinical practice guidelines for symptom control in pediatric oncology. Support Care Cancer 2021;29:7049-55.
35. Signorelli C, Wakefield CE, McLoone JK, et al. ANZCHOG Survivorship Study Group. Models of childhood cancer survivorship care in Australia and New Zealand: strengths and challenges. Asia Pac J Clin Oncol 2017;13:407-15.
37. Hayflick L, Moorhead P. The serial cultivation of human diploid cell strains. Experimental Cell Research 1961;25:585-621.
38. Banerjee P, Kotla S, Reddy Velatooru L, et al. Senescence-associated secretory phenotype as a hinge between cardiovascular diseases and cancer. Front Cardiovasc Med 2021;8:763930.
39. Dominic A, Banerjee P, Hamilton DJ, Le NT, Abe JI. Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis. Redox Biol 2020;37:101614.
40. Liu J, Wang L, Wang Z, Liu JP. Roles of telomere biology in cell senescence, replicative and chronological ageing. Cells 2019;8:54.
41. Chuenwisad K, More-Krong P, Tubsaeng P, et al. Premature senescence and telomere shortening induced by oxidative stress from oxalate, calcium oxalate monohydrate, and urine from patients with calcium oxalate nephrolithiasis. Front Immunol 2021;12:696486.
42. Magalhães JP, Chainiaux F, Remacle J, Toussaint O. Stress-induced premature senescence in BJ and hTERT-BJ1 human foreskin fibroblasts. FEBS Letters 2002;523:157-62.
43. Hewitt G, Jurk D, Marques FD, et al. Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. Nat Commun 2012;3:708.
44. Naka K, Tachibana A, Ikeda K, Motoyama N. Stress-induced premature senescence in hTERT-expressing ataxia telangiectasia fibroblasts. J Biol Chem 2004;279:2030-7.
45. Nakamura AJ, Chiang YJ, Hathcock KS, et al. Both telomeric and non-telomeric DNA damage are determinants of mammalian cellular senescence. Epigenetics Chromatin 2008;1:6.
46. Gioia U, Francia S, Cabrini M, et al. Pharmacological boost of DNA damage response and repair by enhanced biogenesis of DNA damage response RNAs. Sci Rep 2019;9:6460.
47. Schumann S, Scherthan H, Pfestroff K, et al. DNA damage and repair in peripheral blood mononuclear cells after internal ex vivo irradiation of patient blood with 131 I. Eur J Nucl Med Mol Imaging 2022;49:1447-55.
48. Fumagalli M, Rossiello F, Clerici M, et al. Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation. Nat Cell Biol 2012;14:355-65.
49. Vaiserman A, Krasnienkov D. Telomere length as a marker of biological age: state-of-the-art, open issues, and future perspectives. Front Genet 2020;11:630186.
51. Li P, Hou M, Lou F, Björkholm M, Xu D. Telomere dysfunction induced by chemotherapeutic agents and radiation in normal human cells. Int J Biochem Cell Biol 2012;44:1531-40.
52. Wong KK, Maser RS, Bachoo RM, et al. Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing. Nature 2003;421:643-8.
53. Armanios M, Alder JK, Parry EM, Karim B, Strong MA, Greider CW. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am J Hum Genet 2009;85:823-32.
54. Armanios M, Alder JK, Parry EM, Karim B, Strong MA, Greider CW. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am J Hum Genet 2009;85:823-32.
55. Rolles B, Gorgulho J, Tometten M, et al. Telomere shortening in peripheral leukocytes is associated with poor survival in cancer patients treated with immune checkpoint inhibitor therapy. Front Oncol 2021;11:729207.
56. Bianchi A, Smith S, Chong L, Elias P, de Lange T. TRF1 is a dimer and bends telomeric DNA. EMBO J 1997;16:1785-94.
57. Ilicheva NV, Podgornaya OI, Voronin AP. Telomere repeat-binding factor 2 is responsible for the telomere attachment to the nuclear membrane. Elsevier; 2015. pp. 67-96.
58. Kotla S, Vu HT, Ko KA, et al. Endothelial senescence is induced by phosphorylation and nuclear export of telomeric repeat binding factor 2-interacting protein. JCI Insight 2019;4:124867.
59. Gu P, Jia S, Takasugi T, et al. Distinct functions of POT1 proteins contribute to the regulation of telomerase recruitment to telomeres. Nat Commun 2021;12:5514.
60. Liu B, He Y, Wang Y, Song H, Zhou ZH, Feigon J. Structure of active human telomerase with telomere shelterin protein TPP1. Nature 2022;604:578-83.
61. Abe J, Martin JF, Yeh ET. The future of onco-cardiology: we are not just ‘side effect hunters’. Circ Res 2016;119:896-9.
62. Kim SH, Kaminker P, Campisi J. TIN2, a new regulator of telomere length in human cells. Nat Genet 1999;23:405-12.
63. Rossiello F, Aguado J, Sepe S, et al. DNA damage response inhibition at dysfunctional telomeres by modulation of telomeric DNA damage response RNAs. Nat Commun 2017;8:13980.
64. Cipressa F, Cenci G. DNA damage response, checkpoint activation and dysfunctional telomeres: face to face between mammalian cells and Drosophila. Tsitologiia 2013;55:211-7.
65. Guo X, Deng Y, Lin Y, et al. Dysfunctional telomeres activate an ATM-ATR-dependent DNA damage response to suppress tumorigenesis. EMBO J 2007;26:4709-19.
66. Longhese MP. DNA damage response at functional and dysfunctional telomeres. Genes Dev 2008;22:125-40.
67. Muraki K, Murnane JP. The DNA damage response at dysfunctional telomeres, and at interstitial and subtelomeric DNA double-strand breaks. Genes Genet Syst 2018;92:135-52.
69. Passos JF, Nelson G, Wang C, et al. Feedback between p21 and reactive oxygen production is necessary for cell senescence. Mol Syst Biol 2010;6:347.
70. Anderson R, Lagnado A, Maggiorani D, et al. Length-independent telomere damage drives post-mitotic cardiomyocyte senescence. EMBO J 2019;38:e100492.
71. Brand T. Length doesn’t matter-telomere damage triggers cellular senescence in the ageing heart. EMBO J 2019;38:e101571.
72. Li A, Gao M, Jiang W, Qin Y, Gong G. Mitochondrial dynamics in adult cardiomyocytes and heart diseases. Front Cell Dev Biol 2020;8:584800.
73. Livingston K, Schlaak RA, Puckett LL, Bergom C. The role of mitochondrial dysfunction in radiation-induced heart disease: from bench to bedside. Front Cardiovasc Med 2020;7:20.
74. Gorini S, De Angelis A, Berrino L, Malara N, Rosano G, Ferraro E. Chemotherapeutic drugs and mitochondrial dysfunction: focus on doxorubicin, trastuzumab, and sunitinib. Oxidative Medicine and Cellular Longevity 2018;2018:1-15.
75. Wang B, Kohli J, Demaria M. Senescent cells in cancer therapy: friends or foes? Trends Cancer 2020;6:838-57.
76. Wang Y, Boerma M, Zhou D. Ionizing radiation-induced endothelial cell senescence and cardiovascular diseases. Radiat Res 2016;186:153-61.
77. Kotla S, Zhang A, Imanishi M, et al. Nucleus-mitochondria positive feedback loop formed by ERK5 S496 phosphorylation-mediated poly (ADP-ribose) polymerase activation provokes persistent pro-inflammatory senescent phenotype and accelerates coronary atherosclerosis after chemo-radiation. Redox Biol 2021;47:102132.
78. Hodjat M, Haller H, Dumler I, Kiyan Y. Urokinase receptor mediates doxorubicin-induced vascular smooth muscle cell senescence via proteasomal degradation of TRF2. J Vasc Res 2013;50:109-23.
79. Piegari E, De Angelis A, Cappetta D, et al. Doxorubicin induces senescence and impairs function of human cardiac progenitor cells. Basic Res Cardiol 2013;108:334.
80. Chagastelles PC, Nardi NB. Biology of stem cells: an overview. Kidney Int Suppl (2011) 2011;1:63-7.
81. Rebelo-Marques A, De Sousa Lages A, Andrade R, et al. Aging hallmarks: the benefits of physical exercise. Front Endocrinol (Lausanne) 2018;9:258.
82. Rossi DJ, Jamieson CH, Weissman IL. Stems cells and the pathways to aging and cancer. Cell 2008;132:681-96.
83. Kollman C, Howe CW, Anasetti C, et al. Donor characteristics as risk factors in recipients after transplantation of bone marrow from unrelated donors: the effect of donor age. Blood 2001;98:2043-51.
84. Cupit-Link MC, Arora M, Wood WA, Hashmi SK. Relationship between Aging and Hematopoietic Cell Transplantation. Biol Blood Marrow Transplant 2018;24:1965-70.
85. Lahav M, Uziel O, Kestenbaum M, et al. Nonmyeloablative conditioning does not prevent telomere shortening after allogeneic stem cell transplantation. Transplantation 2005;80:969-76.
86. Beauséjour C. Bone marrow-derived cells: the influence of aging and cellular senescence. Handb Exp Pharmacol 2007;180:67-88.
87. Biran A, Krizhanovsky V. Senescent cells talk frankly with their neighbors. Cell Cycle 2015;14:2181-2.
88. Gorgoulis V, Adams PD, Alimonti A, et al. Cellular senescence: defining a path forward. Cell 2019;179:813-27.
89. Kuilman T, Peeper DS. Senescence-messaging secretome: SMS-ing cellular stress. Nat Rev Cancer 2009;9:81-94.
90. Coppé JP, Patil CK, Rodier F, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol 2008;6:2853-68.
91. Wiley CD, Campisi J. The metabolic roots of senescence: mechanisms and opportunities for intervention. Nat Metab 2021;3:1290-301.
92. Sabbatinelli J, Prattichizzo F, Olivieri F, Procopio AD, Rippo MR, Giuliani A. Where metabolism meets senescence: focus on endothelial cells. Front Physiol 2019;10:1523.
93. James EL, Michalek RD, Pitiyage GN, et al. Senescent human fibroblasts show increased glycolysis and redox homeostasis with extracellular metabolomes that overlap with those of irreparable DNA damage, aging, and disease. J Proteome Res 2015;14:1854-71.
94. Chen JH, Ozanne SE. Deep senescent human fibroblasts show diminished DNA damage foci but retain checkpoint capacity to oxidative stress. FEBS Lett 2006;580:6669-73.
95. Zwerschke W, Mazurek S, Stöckl P, Hütter E, Eigenbrodt E, Jansen-Dürr P. Metabolic analysis of senescent human fibroblasts reveals a role for AMP in cellular senescence. Biochem J 2003;376:403-11.
96. Xie N, Zhang L, Gao W, et al. NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential. Signal Transduct Target Ther 2020;5:227.
97. Xiao W, Wang RS, Handy DE, Loscalzo J. NAD(H) and NADP(H) redox couples and cellular energy metabolism. Antioxid Redox Signal 2018;28:251-72.
98. Nacarelli T, Lau L, Fukumoto T, et al. NAD+ metabolism governs the proinflammatory senescence-associated secretome. Nat Cell Biol 2019;21:397-407.
99. Covarrubias AJ, Perrone R, Grozio A, Verdin E. NAD+ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol 2021;22:119-41.
100. Lin Q, Zuo W, Liu Y, Wu K, Liu Q. NAD+ and cardiovascular diseases. Clin Chim Acta 2021;515:104-10.
101. Luongo TS, Eller JM, Lu MJ, et al. SLC25A51 is a mammalian mitochondrial NAD+ transporter. Nature 2020;588:174-9.
102. Leverve XM, Verhoeven AJ, Groen AK, Meijer AJ, Tager JM. The malate/aspartate shuttle and pyruvate kinase as targets involved in the stimulation of gluconeogenesis by phenylephrine. Eur J Biochem 1986;155:551-6.
103. Lautrup S, Sinclair DA, Mattson MP, Fang EF. NAD+ in Brain Aging and Neurodegenerative Disorders. Cell Metab 2019;30:630-55.
104. Braidy N, Guillemin GJ, Mansour H, Chan-Ling T, Poljak A, Grant R. Age related changes in NAD+ metabolism oxidative stress and Sirt1 activity in wistar rats. PLoS One 2011;6:e19194.
105. Camacho-Pereira J, Tarragó MG, Chini CCS, et al. CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metab 2016;23:1127-39.
106. Mouchiroud L, Houtkooper RH, Moullan N, et al. The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling. Cell 2013;154:430-41.
107. Zhu XH, Lu M, Lee BY, Ugurbil K, Chen W. In vivo NAD assay reveals the intracellular NAD contents and redox state in healthy human brain and their age dependences. Proc Natl Acad Sci U S A 2015;112:2876-81.
109. Zhang H, Ryu D, Wu Y, et al. NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice. Science 2016;352:1436-43.
110. Frederick DW, Loro E, Liu L, et al. Loss of NAD homeostasis leads to progressive and reversible degeneration of skeletal muscle. Cell Metab 2016;24:269-82.
111. Stein LR, Imai S. Specific ablation of Nampt in adult neural stem cells recapitulates their functional defects during aging. EMBO J 2014;33:1321-40.
112. van der Veer E, Ho C, O’Neil C, et al. Extension of human cell lifespan by nicotinamide phosphoribosyltransferase. J Biol Chem 2007;282:10841-5.
113. Chang HC, Guarente L. SIRT1 mediates central circadian control in the SCN by a mechanism that decays with aging. Cell 2013;153:1448-60.
114. Zeidler JD, Hogan KA, Agorrody G, et al. The CD38 glycohydrolase and the NAD sink: implications for pathological conditions. Am J Physiol Cell Physiol 2022;322:C521-45.
115. Chini CCS, Zeidler JD, Kashyap S, Warner G, Chini EN. Evolving concepts in NAD+ metabolism. Cell Metab 2021;33:1076-87.
116. Feldman JL, Dittenhafer-Reed KE, Denu JM. Sirtuin catalysis and regulation. J Biol Chem 2012;287:42419-27.
117. Pehar M, Harlan BA, Killoy KM, Vargas MR. Nicotinamide adenine dinucleotide metabolism and neurodegeneration. Antioxid Redox Signal 2018;28:1652-68.
118. Hayakawa T, Iwai M, Aoki S, et al. SIRT1 suppresses the senescence-associated secretory phenotype through epigenetic gene regulation. PLoS One 2015;10:e0116480.
119. Lee S, Lee J, Lee H, Min K. Sirtuin signaling in cellular senescence and aging. BMB Rep 2019;52:24-34.
120. Mostoslavsky R, Chua KF, Lombard DB, et al. Genomic instability and aging-like phenotype in the absence of mammalian SIRT6. Cell 2006;124:315-29.
121. Ota H, Akishita M, Eto M, Iijima K, Kaneki M, Ouchi Y. Sirt1 modulates premature senescence-like phenotype in human endothelial cells. J Mol Cell Cardiol 2007;43:571-9.
122. Kane AE, Sinclair DA. Sirtuins and NAD+ in the Development and treatment of metabolic and cardiovascular diseases. Circ Res 2018;123:868-85.
123. Murata MM, Kong X, Moncada E, et al. NAD+ consumption by PARP1 in response to DNA damage triggers metabolic shift critical for damaged cell survival. Mol Biol Cell 2019;30:2584-97.
124. Poltronieri P, Celetti A, Palazzo L. Mono(ADP-ribosyl)ation enzymes and NAD+ metabolism: a focus on diseases and therapeutic perspectives. Cells 2021;10:128.
125. Jubin T, Kadam A, Jariwala M, et al. The PARP family: insights into functional aspects of poly (ADP-ribose) polymerase-1 in cell growth and survival. Cell Prolif 2016;49:421-37.
126. Savelyev NV, Shepelev NM, Lavrik OI, Rubtsova MP, Dontsova OA. PARP1 regulates the biogenesis and activity of telomerase complex through modification of H/ACA-proteins. Front Cell Dev Biol 2021;9:621134.
127. Gomez M, Wu J, Schreiber V, et al. PARP1 Is a TRF2-associated poly(ADP-ribose)polymerase and protects eroded telomeres. Mol Biol Cell 2006;17:1686-96.
128. Gupte R, Liu Z, Kraus WL. PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes. Genes Dev 2017;31:101-26.
130. Ohanna M, Giuliano S, Bonet C, et al. Senescent cells develop a PARP-1 and nuclear factor-{kappa}B-associated secretome (PNAS). Genes Dev 2011;25:1245-61.
131. Lv ZC, Li F, Wang L, et al. Impact of parthanatos on the increased risk of onset and mortality in male patients with pulmonary hypertension. Am J Mens Health 2021;15:15579883211029458.
132. Malyuchenko NV, Kotova EY, Kulaeva OI, Kirpichnikov MP, Studitskiy VM. PARP1 inhibitors: antitumor drug design. Acta Naturae 2015;7:27-37.
133. Quarona V, Zaccarello G, Chillemi A, et al. CD38 and CD157: a long journey from activation markers to multifunctional molecules. Cytometry B Clin Cytom 2013;84:207-17.
134. Hogan KA, Chini CCS, Chini EN. The multi-faceted ecto-enzyme CD38: Roles in immunomodulation, cancer, aging, and metabolic diseases. Front Immunol 2019;10:1187.
135. Preugschat F, Carter LH, Boros EE, Porter DJ, Stewart EL, Shewchuk LM. A pre-steady state and steady state kinetic analysis of the N-ribosyl hydrolase activity of hCD157. Arch Biochem Biophys 2014;564:156-63.
136. Chini CCS, Peclat TR, Warner GM, et al. CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. Nat Metab 2020;2:1284-304.
137. Tarragó MG, Chini CCS, Kanamori KS, et al. A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline. Cell Metab 2018;27:1081-1095.e10.
138. Covarrubias AJ, Kale A, Perrone R, et al. Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages. Nat Metab 2020;2:1265-83.
139. Boslett J, Hemann C, Christofi FL, Zweier JL. Characterization of CD38 in the major cell types of the heart: endothelial cells highly express CD38 with activation by hypoxia-reoxygenation triggering NAD(P)H depletion. Am J Physiol Cell Physiol 2018;314:C297-309.
140. Agorrody G, Peclat TR, Peluso G, et al. Benefits in cardiac function by CD38 suppression: Improvement in NAD+ levels, exercise capacity, heart rate variability and protection against catecholamine-induced ventricular arrhythmias. J Mol Cell Cardiol 2022;166:11-22.
141. Boslett J, Hemann C, Zhao YJ, Lee HC, Zweier JL. Luteolinidin protects the postischemic heart through CD38 Inhibition with preservation of NAD(P)(H). J Pharmacol Exp Ther 2017;361:99-108.
142. Boslett J, Reddy N, Alzarie YA, Zweier JL. Inhibition of CD38 with the Thiazoloquin(az)olin(on)e 78c Protects the heart against postischemic injury. J Pharmacol Exp Ther 2019;369:55-64.
143. Hopkins EL, Gu W, Kobe B, Coleman MP. A Novel NAD Signaling Mechanism in Axon Degeneration and its Relationship to Innate Immunity. Front Mol Biosci 2021;8:703532.
144. Gerdts J, Brace EJ, Sasaki Y, DiAntonio A, Milbrandt J. SARM1 activation triggers axon degeneration locally via NAD+ destruction. Science 2015;348:453-7.
145. Wang Q, Zhang S, Liu T, et al. Sarm1/Myd88-5 regulates neuronal intrinsic immune response to traumatic axonal injuries. Cell Rep 2018;23:716-24.
146. Murata H, Khine CC, Nishikawa A, Yamamoto KI, Kinoshita R, Sakaguchi M. c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration. J Biol Chem 2018;293:18933-43.
147. Gilley J, Ribchester RR, Coleman MP. Sarm1 deletion, but not WldS, confers lifelong rescue in a mouse model of severe axonopathy. Cell Rep 2017;21:10-6.
148. Sur M, Dey P, Sarkar A, et al. Sarm1 induction and accompanying inflammatory response mediates age-dependent susceptibility to rotenone-induced neurotoxicity. Cell Death Discov 2018;4:114.
149. Liu HW, Smith CB, Schmidt MS, et al. Pharmacological bypass of NAD+ salvage pathway protects neurons from chemotherapy-induced degeneration. Proc Natl Acad Sci U S A 2018;115:10654-9.
150. Mukherjee P, Woods TA, Moore RA, Peterson KE. Activation of the innate signaling molecule MAVS by bunyavirus infection upregulates the adaptor protein SARM1, leading to neuronal death. Immunity 2013;38:705-16.
151. Osterloh JM, Yang J, Rooney TM, et al. dSarm/Sarm1 is required for activation of an injury-induced axon death pathway. Science 2012;337:481-4.
152. Lin CW, Liu HY, Chen CY, Hsueh YP. Neuronally-expressed Sarm1 regulates expression of inflammatory and antiviral cytokines in brains. Innate Immun 2014;20:161-72.
153. Yoo KH, Tang JJ, Rashid MA, et al. Nicotinamide mononucleotide prevents cisplatin-induced cognitive impairments. Cancer Res 2021;81:3727-37.
154. Navas LE, Carnero A. NAD+ metabolism, stemness, the immune response, and cancer. Signal Transduct Target Ther 2021;6:2.
155. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell 2013;153:1194-217.
156. Franceschi C, Bonafè M, Valensin S, et al. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci 2000;908:244-54.
157. Chini C, Hogan KA, Warner GM, et al. The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD+ decline. Biochem Biophys Res Commun 2019;513:486-93.
158. Cameron AM, Castoldi A, Sanin DE, et al. Inflammatory macrophage dependence on NAD+ salvage is a consequence of reactive oxygen species-mediated DNA damage. Nat Immunol 2019;20:420-32.
159. Muris Consortium, Overall coordination, Logistical coordination, Organ collection and processing, Library preparation and sequencing, Computational data analysis, Cell type annotation, Writing group, Supplemental text writing group, Principal investigators. Single-cell transcriptomics of 20 mouse organs creates a tabula Muris. Nature 2018;562:367-72.
160. Youm YH, Grant RW, McCabe LR, et al. Canonical Nlrp3 inflammasome links systemic low-grade inflammation to functional decline in aging. Cell Metab 2013;18:519-32.
161. Jeng MY, Hull PA, Fei M, et al. Metabolic reprogramming of human CD8+ memory T cells through loss of SIRT1. J Exp Med 2018;215:51-62.
162. Chatterjee S, Daenthanasanmak A, Chakraborty P, et al. CD38-NAD+axis regulates immunotherapeutic anti-tumor T cell response. Cell Metab 2018;27:85-100.e8.
163. Lee KA, Shin KS, Kim GY, et al. Characterization of age-associated exhausted CD8+ T cells defined by increased expression of Tim-3 and PD-1. Aging Cell 2016;15:291-300.
164. Shimada Y, Hayashi M, Nagasaka Y, Ohno-Iwashita Y, Inomata M. Age-associated up-regulation of a negative co-stimulatory receptor PD-1 in mouse CD4+ T cells. Exp Gerontol 2009;44:517-22.
165. Lages CS, Lewkowich I, Sproles A, Wills-Karp M, Chougnet C. Partial restoration of T-cell function in aged mice by in vitro blockade of the PD-1/ PD-L1 pathway. Aging Cell 2010;9:785-98.
166. Wang Y, Wang F, Wang L, et al. NAD+ supplement potentiates tumor-killing function by rescuing defective TUB-mediated NAMPT transcription in tumor-infiltrated T cells. Cell Rep 2021;36:109516.
167. Verma V, Shrimali RK, Ahmad S, et al. PD-1 blockade in subprimed CD8 cells induces dysfunctional PD-1+ CD38hi cells and anti-PD-1 resistance. Nat Immunol 2019;20:1231-43.
168. Chen L, Diao L, Yang Y, et al. CD38-Mediated immunosuppression as a mechanism of tumor cell escape from PD-1/PD-L1 blockade. Cancer Discov 2018;8:1156-75.
169. Kumar N, Qian W, Van Houten B. Sick mitochondria cause telomere damage: implications for disease. Mol Cell Oncol 2020;7:1678362.
170. Bai P. Biology of poly(ADP-Ribose) polymerases: the factotums of cell maintenance. Mol Cell 2015;58:947-58.
171. Alano CC, Garnier P, Ying W, Higashi Y, Kauppinen TM, Swanson RA. NAD+ depletion is necessary and sufficient for poly(ADP-ribose) polymerase-1-mediated neuronal death. J Neurosci 2010;30:2967-78.
172. Tang KS, Suh SW, Alano CC, et al. Astrocytic poly(ADP-ribose) polymerase-1 activation leads to bioenergetic depletion and inhibition of glutamate uptake capacity. Glia 2010;58:446-57.
173. Bai P, Cantó C, Oudart H, et al. PARP-1 inhibition increases mitochondrial metabolism through SIRT1 activation. Cell Metab 2011;13:461-8.
174. Virag L, Salzman AL, Szabo C. Poly(ADP-ribose) synthetase activation mediates mitochondrial injury during oxidant-induced cell death. J Immunol 1998;161:3753-9.
175. Bai P, Nagy L, Fodor T, Liaudet L, Pacher P. Poly(ADP-ribose) polymerases as modulators of mitochondrial activity. Trends Endocrinol Metab 2015;26:75-83.
176. Singh MV, Kotla S, Le NT, et al. Senescent phenotype induced by p90RSK-NRF2 signaling sensitizes monocytes and macrophages to oxidative stress in HIV-positive individuals. Circulation 2019;139:1199-216.
177. Albadawi H, Crawford RS, Atkins MD, Watkins MT. Role of poly(ADP-ribose) polymerase during vascular reconstruction. Vascular 2006;14:362-5.
178. Yeh JM, Ward ZJ, Chaudhry A, et al. Life expectancy of adult survivors of childhood cancer over 3 decades. JAMA Oncol 2020;6:350-7.
179. Miller KD, Nogueira L, Mariotto AB, et al. Cancer treatment and survivorship statistics, 2019. CA Cancer J Clin 2019;69:363-85.
180. Bluethmann SM, Mariotto AB, Rowland JH. Anticipating the “Silver Tsunami”: prevalence trajectories and comorbidity burden among older cancer survivors in the United States. Cancer Epidemiol Biomarkers Prev 2016;25:1029-36.
181. Sedrak MS, Kirkland JL, Tchkonia T, Kuchel GA. Accelerated aging in older cancer survivors. J Am Geriatr Soc 2021;69:3077-80.
182. Kannel WB, Dawber TR, Kagan A, Revotskie N, Stokes J 3rd. Factors of risk in the development of coronary heart disease--six year follow-up experience. The Framingham Study. Ann Intern Med 1961;55:33-50.
183. Stern S, Behar S, Gottlieb S. Cardiology patient pages. Aging and diseases of the heart. Circulation 2003;108:e99-101.
184. Kincaid JW, Berger NA. NAD metabolism in aging and cancer. Exp Biol Med (Maywood) 2020;245:1594-614.
185. Oeffinger KC, Mertens AC, Sklar CA, et al. Childhood Cancer Survivor Study. Chronic health conditions in adult survivors of childhood cancer. N Engl J Med 2006;355:1572-82.
186. Khanna A, Pequeno P, Gupta S, et al. Increased risk of all cardiovascular disease subtypes among childhood cancer survivors: population-based matched cohort study. Circulation 2019;140:1041-3.
187. von Korn P, Müller J, Quell C, et al. Health-related physical fitness and arterial stiffness in childhood cancer survivors. Front Cardiovasc Med 2019;6:63.
188. Vatanen A, Hou M, Huang T, et al. Clinical and biological markers of premature aging after autologous SCT in childhood cancer. Bone Marrow Transplant 2017;52:600-5.
189. Guida JL, Ahles TA, Belsky D, et al. Measuring aging and identifying aging phenotypes in cancer survivors. J Natl Cancer Inst 2019;111:1245-54.
190. Gold K, Gaharwar AK, Jain A. Emerging trends in multiscale modeling of vascular pathophysiology: Organ-on-a-chip and 3D printing. Biomaterials 2019;196:2-17.
191. Walther BK, Rajeeva Pandian NK, Gold KA, et al. Mechanotransduction-on-chip: vessel-chip model of endothelial YAP mechanobiology reveals matrix stiffness impedes shear response. Lab Chip 2021;21:1738-51.
192. Saha B, Mathur T, Tronolone JJ, et al. Human tumor microenvironment chip evaluates the consequences of platelet extravasation and combinatorial antitumor-antiplatelet therapy in ovarian cancer. Sci Adv 2021;7:eabg5283.
193. Mathur T, Flanagan JM, Jain A. Tripartite collaboration of blood-derived endothelial cells, next generation RNA sequencing and bioengineered vessel-chip may distinguish vasculopathy and thrombosis among sickle cell disease patients. Bioeng Transl Med 2021;6:e10211.
194. Gold KA, Saha B, Rajeeva Pandian NK, et al. 3D bioprinted multicellular vascular models. Adv Healthc Mater 2021;10:e2101141.
195. Pandian NK, Walther BK, Suresh R, Cooke JP, Jain A. Microengineered human vein-chip recreates venous valve architecture and its contribution to thrombosis. Small 2020;16:e2003401.
