References
[1] Vanhooren V, Libert C. The mouse as a model organism in aging research: usefulness, pitfalls and possibilities [J]. Ageing Res Rev, 2013, 12(1): 8-21.
[2] Harkema L, Youssef S A, De Bruin A. Pathology of Mouse Models of Accelerated Aging [J]. Vet Pathol, 2016, 53(2): 366-89.
[3] Fried L P, Tangen C M, Walston J, et al. Frailty in older adults: evidence for a phenotype [J]. J Gerontol A Biol Sci Med Sci, 2001, 56(3): M146-56.
[4] Whitehead J C, Hildebrand B A, Sun M, et al. A clinical frailty index in aging mice: comparisons with frailty index data in humans [J]. J Gerontol A Biol Sci Med Sci, 2014, 69(6): 621-32.
[5] Wang T, Di G, Yang L, et al. Saponins from Panax japonicus attenuate D-galactose-induced cognitive impairment through its anti-oxidative and anti-apoptotic effects in rats [J]. J Pharm Pharmacol, 2015, 67(9): 1284-96.
[6] De Souza Silva M A, Lenz B, Rotter A, et al. Neurokinin3 receptor as a target to predict and improve learning and memory in the aged organism [J]. Proc Natl Acad Sci U S A, 2013, 110(37): 15097-102.
[7] Wang W, Li S, Dong H P, et al. Differential impairment of spatial and nonspatial cognition in a mouse model of brain aging [J]. Life Sci, 2009, 85(3-4): 127-35.
[8] Dimri G P, Lee X, Basile G, et al. A biomarker that identifies senescent human cells in culture and in aging skin in vivo [J]. Proc Natl Acad Sci U S A, 1995, 92(20): 9363-7.
[9] Coppé J P, Patil C K, Rodier F, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor [J]. PLoS Biol, 2008, 6(12): 2853-68.
[10] Harman D. Aging: a theory based on free radical and radiation chemistry [J]. J Gerontol, 1956, 11(3): 298-300.
[11] Hekimi S, Lapointe J, Wen Y. Taking a "good" look at free radicals in the aging process [J]. Trends Cell Biol, 2011, 21(10): 569-76.
[12] Quintanilla R A, Orellana D I, González-Billault C, et al. Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway [J]. Exp Cell Res, 2004, 295(1): 245-57.
[13] Chiba Y, Shimada A, Kumagai N, et al. The senescence-accelerated mouse (SAM): a higher oxidative stress and age-dependent degenerative diseases model [J]. Neurochem Res, 2009, 34(4): 679-87.
[14] Shcherbakov D, Nigri M, Akbergenov R, et al. Premature aging in mice with error-prone protein synthesis [J]. Sci Adv, 2022, 8(9): eabl9051.
[15] Shwe T, Pratchayasakul W, Chattipakorn N, et al. Role of D-galactose-induced brain aging and its potential used for therapeutic interventions [J]. Exp Gerontol, 2018, 101: 13-36.
[16] Azman K F, Zakaria R. D-Galactose-induced accelerated aging model: an overview [J]. Biogerontology, 2019, 20(6): 763-82.
[17] Vasu V T, Oommen S, Lim Y, et al. Modulation of ozone-sensitive genes in alpha-tocopherol transfer protein null mice [J]. Inhal Toxicol, 2010, 22(1): 1-16.
[18] Robison L L, Hudson M M. Survivors of childhood and adolescent cancer: life-long risks and responsibilities [J]. Nat Rev Cancer, 2014, 14(1): 61-70.
[19] Fielder E, Weigand M, Agneessens J, et al. Sublethal whole-body irradiation causes progressive premature frailty in mice [J]. Mech Ageing Dev, 2019, 180: 63-9.
[20] Grosse L, Wagner N, Emelyanov A, et al. Defined p16(High) Senescent Cell Types Are Indispensable for Mouse Healthspan [J]. Cell Metab, 2020, 32(1): 87-99.e6.
[21] Omori S, Wang T W, Johmura Y, et al. Generation of a p16 Reporter Mouse and Its Use to Characterize and Target p16(high) Cells In Vivo [J]. Cell Metab, 2020, 32(5): 814-28.e6.