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参考文献
[1]Christensen K, Doblhammer G, Rau R. Ageing populations:the challenges ahead. Lancet, 2009, 374(9696):1196-1208.
[2]Kenyon CJ. The genetics of ageing. Nature, 2010, 464(7288):504-512.
[3]Guarente L. Mitochondria — a nexus for aging, calorie restriction, and sirtuins? Cell, 2008, 132(2):171-176.
[4]Haigis MC, Yankner BA. The aging stress response. Mol Cell, 2010, 40(2):333-344.
[5]Matoba S, Kang JG, Patino WD, et al. p53 regulates mitochondrial respiration. Science, 2006, 312(5780):1650-1653.
[6]Ventura N, Rea SL, Schiavi A, et al. p53/CEP-1 increases or decreases lifespan, depending on level of mitochondrial bioenergetic stress. Aging Cell, 2009, 8(4):380-393.
[7]Feng Z, Levine AJ. The regulation of energy metabolism and the IGF-1/mTOR pathways by the p53 protein. Trends Cell Biol, 2010, 20(7):427-434.
[8]Hinkal G, Donehower LA. How does suppression of IGF-1 signaling by DNA damage affect aging and longevity? Mech Ageing Dev, 2008, 129(5):243-253.
[9]Sahin E, Colla S, Liesa M, et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature, 2011, 470(7334):359-365.
[10]Harrison DE, Strong R, Sharp ZD, et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature, 2009, 460(7253):392-395.
[11]Chiacchiera F, Simone C. The AMPK — FoxO3A axis as a target for cancer treatment. Cell Cycle, 2010, 9(6):1091-1096.
[12]Canto C, Auwerx J. PGC-1α, SIRT1 and AMPK, an energy sensing network that controls energy expenditure. Curr Opin Lipidol, 2009, 20(2):98-105.
[13]Puigserver P, Rhee J, Donovan J, et al. Insulin-regulated hepatic gluconeogenesis through FOXO1-PGC-1α interaction. Nature, 2003, 423(6936):550-555.
[14]Sadagurski M, Cheng Z, Rozzo A, et al. IRS2 increases mitochondrial dysfunction and oxidative stress in a mouse model of Huntington disease. J Clin Invest, 2011, 121(10):4070-4081.
[15]Paik JH, Ding Z, Narurkar R, et al. FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis. Cell Stem Cell, 2009, 5(5):540-553.
[16]Zid BM, Rogers AN, Katewa SD, et al. 4E-BP extends lifespan upon dietary restriction by enhancing mitochondrial activity in Drosophila. Cell, 2009, 139(1):149-160.
[17]Selman C, Tullet JM, Wieser D, et al. Ribosomal protein S6 kinase 1 signaling regulates mammalian life span. Science, 2009, 326(5949):140-144.
[18]Canto C, Gerhart-Hines Z, Feige JN, et al. AMPK regulates energy expenditure by modulating NAD + metabolism and SIRT1 activity. Nature, 2009, 458(7241):1056-1060.
[19]Trifunovic A, Wredenberg A, Falkenberg M, et al. Premature ageing in mice expressing defective mitochondrial DNA polymerase. Nature, 2004, 429(6990):417-423.
[20]Liu X, Jiang N, Hughes B, et al. Evolutionary conservation of the clk-1-dependent mechanism of longevity: loss of mclk1 increases cellular fitness and lifespan in mice. Genes Dev, 2005, 19(20):2424-2434.
[21]Jones RG, Plas DR, Kubek S, et al. AMP-activated protein kinase induces a p53-dependent metabolic checkpoint. Mol Cell, 2005, 18(3):283-293.
[22]Sung JY, Woo CH, Kang YJ, et al. AMPK induces vascular smooth muscle cell senescence via LKB1 dependent pathway. Biochem Biophys Res Commun, 2011, 413(1):143-148.
[23]Calado RT, Young NS. Telomere diseases. N Engl J Med, 2009, 361(24):2353-2365.
[24]Martin GM. Genetic modulation of senescent phenotypes in Homo sapiens. Cell, 2005, 120(4):523-532.
[25]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.
[26]Hao LY, Armanios M, Strong MA, et al. Short telomeres, even in the presence of telomerase, limit tissue renewal capacity. Cell, 2005, 123(6):1121-1131.
[27]Tomas-Loba A, Flores I, Fernández-Marcos PJ, et al. Telomerase reverse transcriptase delays aging in cancer-resistant mice. Cell, 2008, 135(4):609-622.
[28]Chang S, Multani AS, Cabrera NG, et al. Essential role of limiting telomeres in the pathogenesis of Werner syndrome. Nat Genet, 2004, 36(8):877-882.
[29]Jaskelioff M, Muller FL, Paik JH, et al. Telomerase reactivation reverses tissue degeneration in aged telomerased eficient mice. Nature, 2011, 469(7328):102-106.
[30]Sharpless NE, DePinho RA. Telomeres, stem cells, senescence, and cancer. J Clin Invest, 2004, 113(2): 160-168.
[31]Choudhury AR, Ju Z, Djojosubroto MW, et al. Cdkn1a deletion improves stem cell function and lifespan of mice with dysfunctional telomeres without accelerating cancer formation. Nat Genet, 2007, 39(1):99-105.
[32]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.
[33]Guo N, Parry EM, Li LS, et al. Short telomeres compromise β-cell signaling and survival. PLoS ONE, 2011, 6(3):e17858.
[34]Vidal-Cardenas SL, Greider CW. Comparing effects of mTR and mTERT deletion on gene expression and DNA damage response:a critical examination of telomere length maintenanceindependent roles of telomerase. Nucleic Acids Res, 2010, 38(1):60-71.
[35]Sharma NK, Reyes A, Green P, et al. Human telomerase acts as a hTR-independent reverse transcriptase in mitochondria. Nucleic Acids Res, 2011, 40(2):712-725.
[36]Pallardo FV, Lloret A, Lebel M, et al. Mitochondrial dysfunction in some oxidative stress-related genetic diseases:ataxia-telangiectasia, down syndrome, Fanconi anaemia and Werner syndrome. Biogerontology, 2010, 11(4):401-419.
[37]Varela I, Cadi?anos J, Pendás AM, et al. Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation. Nature, 2005, 437(7058):564-568.
[38]Kim WY, Sharpless NE. The regulation of INK4/ARF in cancer and aging. Cell, 2006, 127(2):265-275.
[39]Sahin E, DePinho RA. Axis of ageing:telomeres, p53 and mitochondria. Nat Rev Mol Cell Biol, 2013, 13(6):397-404.
[40]Finkel T, Deng CX, Mostoslavsky R. Recent progress in the biology and physiology of sirtuins. Nature, 2009, 460(7255):587-591.
[41]Burnett C, Valentini S, Cabreiro F, et al. Absence of effects of Sir2 overexpression on lifespan in C. elegans and Drosophila. Nature, 2011, 477(7365):482-485.
[42]Passos JF, Saretzki G, Ahmed S, et al. Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomeredependent senescence. PLoS Biol, 2007, 5(5):e110.
[43]de Jesus BB, Schneeberger K, Vera E, et al. The telomerase activator TA-65 elongates short telomeres and increases health span of adult/old mice without increasing cancer incidence. Aging Cell, 2011, 10(4): 604-621.
[44]Wenz T, Rossi SG, Rotundo RL, et al. Increased muscle PGC-1α expression protects from sarcopenia and metabolic disease during aging. Proc Natl Acad Sci USA, 2009, 106(48):20405-20410.
[45]Little JP, Safdar A, Bishop D, et al. An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol, 2011, 300(6):R1303-R1310.
[46]Timmers S, Konings E, Bilet L, et al. Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans. Cell Metab, 2011, 14(5):612-622.
[47]Hu J, Hwang SS, Liesa M, et al. Antitelomerase therapy provokes ALT and mitochondrial adaptive mechanisms in cancer. Cell, 2012, 148(4):651-663.