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Senolytics and senomorphics: Natural and synthetic therapeutics in the treatment of aging and chronic diseases
Abstract
Cellular senescence is a heterogeneous process guided by genetic, epigenetic and environmental factors, characterizing many types of somatic cells. It has been suggested as an aging hallmark that is believed to contribute to aging and chronic diseases. Senescent cells (SC) exhibit a specific senescence-associated secretory phenotype (SASP), mainly characterized by the production of proinflammatory and matrix-degrading molecules. When SC accumulate, a chronic, systemic, low-grade inflammation, known as inflammaging, is induced. In turn, this chronic immune system activation results in reduced SC clearance thus establishing a vicious circle that fuels inflammaging. SC accumulation represents a causal factor for various age-related pathologies. Targeting of several aging hallmarks has been suggested as a strategy to ameliorate healthspan and possibly lifespan. Consequently, SC and SASP are viewed as potential therapeutic targets either through the selective killing of SC or the selective SASP blockage, through natural or synthetic compounds. These compounds are members of a family of agents called senotherapeutics divided into senolytics and senomorphics. Few of them are already in clinical trials, possibly representing a future treatment of age-related pathologies including diseases such as atherosclerosis, osteoarthritis, osteoporosis, cancer, diabetes, neurodegenerative diseases such as Alzheimer's disease, cardiovascular diseases, hepatic steatosis, chronic obstructive pulmo…
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“Several studies have shown that flavonoids are promising candidates in senescence-related research, hence the importance of finding new and more efficacious compounds of this kind67–69.”
From Discovery of senolytics using machine learning (2023) · cites this paper as [69]
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López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
Telomeres shorten during ageing of human fibroblasts
Harley, C. B., Futcher, A. B., & Greider, C. W. (1990) · Nature · doi:10.1038/345458a0 · Cited by 5,750
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
Extension of Life-Span by Introduction of Telomerase into Normal Human Cells
Bodnar, A. G., Ouellette, M., Frolkis, M., Holt, S. E., Chiu, C.-P., Morin, G. B., Harley, C. B., Shay, J. W., Lichtsteiner, S., & Wright, W. E. (1998) · Science · doi:10.1126/science.279.5349.349 · Cited by 4,975
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
STATs in cancer inflammation and immunity: a leading role for STAT3
Yu, H., Pardoll, D., & Jove, R. (2009) · Nature reviews. Cancer · doi:10.1038/nrc2734 · Cited by 4,383
Itoh, K., Chiba, T., Takahashi, S., Ishii, T., Igarashi, K., Katoh, Y., Oyake, T., Hayashi, N., Satoh, K., Hatayama, I., et al. (1997) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1997.6943 · Cited by 3,999
AMPK Phosphorylation of Raptor Mediates a Metabolic Checkpoint
Gwinn, D. M., Shackelford, D. B., Egan, D. F., Mihaylova, M. M., Mery, A., Vasquez, D. S., Turk, B. E., & Shaw, R. J. (2008) · Molecular Cell · doi:10.1016/j.molcel.2008.03.003 · Cited by 3,849
Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan
Howitz, K. T., Bitterman, K. J., Cohen, H. Y., Lamming, D. W., Lavu, S., Wood, J. G., Zipkin, R. E., Chung, P., Kisielewski, A., Zhang, L.-L., et al. (2003) · Nature · doi:10.1038/nature01960 · Cited by 3,796
Rapamycin fed late in life extends lifespan in genetically heterogeneous mice
Harrison, D. E., Strong, R., Sharp, Z. D., Nelson, J. F., Astle, C. M., Flurkey, K., Nadon, N. L., Wilkinson, J. E., Frenkel, K., Carter, C. S., et al. (2009) · Nature · doi:10.1038/nature08221 · Cited by 3,766
Flagged first, then by citations
Research works printed but not linked: 173
- Kirkwood, 2005, Understanding the odd science of aging, Cell, 120, 437, 10.1016/j.cell.2005.01.027 · DOI · Paper page
- Campisi, 1996, Replicative senescence: an old lives' tale?, Cell, 84, 497, 10.1016/S0092-8674(00)81023-5 · DOI
- Wang, 2009, DNA damage response and cellular senescence in tissues of aging mice, Aging Cell, 8, 311, 10.1111/j.1474-9726.2009.00481.x · DOI · Paper page
- Kirkland, 2013, Translating advances from the basic biology of aging into clinical application, Exp. Gerontol., 48, 1, 10.1016/j.exger.2012.11.014 · DOI · Paper page
- Borghesan, 2020, A senescence-centric view of aging: implications for longevity and disease, Trends Cell Biol., 30, 777, 10.1016/j.tcb.2020.07.002 · DOI · Paper page
- Hayflick, 1961, The serial cultivation of human diploid cell strains, Exp. Cell Res., 25, 585, 10.1016/0014-4827(61)90192-6 · DOI · Paper page
- Ames, 1992, Oxidants are a major contributor to aging, Ann. N. Y. Acad. Sci., 663, 85, 10.1111/j.1749-6632.1992.tb38652.x · DOI
- Frippiat, 2001, Subcytotoxic H2O2 stress triggers a release of transforming growth factor-β1, which induces biomarkers of cellular senescence of human diploid fibroblasts, J. Biol. Chem., 276, 2531, 10.1074/jbc.M006809200 · DOI
- Chondrogianni, 2003, Central role of the proteasome in senescence and survival of human fibroblasts. Induction of a senescence-like phenotype upon its inhibition and resistance to stress upon its activation, J. Biol. Chem., 278, 28026, 10.1074/jbc.M301048200 · DOI
- Chondrogianni, 2004, Proteasome inhibition induces a senescence-like phenotype in primary human fibroblasts cultures, Biogerontology, 5, 55, 10.1023/B:BGEN.0000017687.55667.42 · DOI
- Sies, 2020, Reactive oxygen species (ROS) as pleiotropic physiological signalling agents, Nat. Rev. Mol. Cell Biol., 21, 363, 10.1038/s41580-020-0230-3 · DOI · Paper page
- Moody, 1982, Mutagenicity of oxygen free radicals, Proc. Natl. Acad. Sci. U.S.A., 79, 2855, 10.1073/pnas.79.9.2855 · DOI
- Davalli, 2016, ROS, cell senescence, and novel molecular mechanisms in aging and age-related diseases, Oxid. Med. Cell. Longev., 2016
- Linke, 1996, A reversible, p53-dependent G0/G1 cell cycle arrest induced by ribonucleotide depletion in the absence of detectable DNA damage, Genes Dev., 10, 934, 10.1101/gad.10.8.934 · DOI
- Liu, 2008, Clair, ROS and p53: a versatile partnership, Free Radic. Biol. Med., 44, 1529, 10.1016/j.freeradbiomed.2008.01.011 · DOI
- Eijkelenboom, 2013, FOXOs: signalling integrators for homeostasis maintenance, Nat. Rev. Mol. Cell Biol., 14, 83, 10.1038/nrm3507 · DOI
- Klotz, 2017, Cellular adaptation to xenobiotics: interplay between xenosensors, reactive oxygen species and FOXO transcription factors, Redox Biol, 13, 646, 10.1016/j.redox.2017.07.015 · DOI
- Oliveira-Marques, 2009, Role of hydrogen peroxide in NF-κB activation: from inducer to modulator, Antioxidants Redox Signal., 11, 2223, 10.1089/ars.2009.2601 · DOI
- Brand, 2016, Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling, Free Radic. Biol. Med., 100, 14, 10.1016/j.freeradbiomed.2016.04.001 · DOI · Paper page
- Harman, 1956, Aging: a theory based on free radical and radiation chemistry, J. Gerontol., 11, 298, 10.1093/geronj/11.3.298 · DOI · Paper page
- Doonan, 2008, Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on life span in Caenorhabditis elegans, Genes Dev., 22, 3236, 10.1101/gad.504808 · DOI · Paper page
- Van Remmen, 2004, Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging, Physiol. Genom., 16, 29, 10.1152/physiolgenomics.00122.2003 · DOI · Paper page
- Ristow, 2010, How increased oxidative stress promotes longevity and metabolic health: the concept of mitochondrial hormesis (mitohormesis), Exp. Gerontol., 45, 410, 10.1016/j.exger.2010.03.014 · DOI · Paper page
- Papaevgeniou, 2016, UPS activation in the battle against aging and aggregation-related diseases: an extended review, 10.1007/978-1-4939-3756-1_1 · DOI
- Gioran, 2020, Mitochondria (cross)talk with proteostatic mechanisms: focusing on ageing and neurodegenerative diseases, Mech. Ageing Dev., 190, 111324, 10.1016/j.mad.2020.111324 · DOI
- Vasileiou, 2019, Mitochondrial homeostasis and cellular senescence, Cells, 8, 686, 10.3390/cells8070686 · DOI
- Chapman, 2019, Mitochondrial dysfunction and cell senescence: deciphering a complex relationship, FEBS Lett., 593, 1566, 10.1002/1873-3468.13498 · DOI · Paper page
- Storer, 2013, XSenescence is a developmental mechanism that contributes to embryonic growth and patterning, Cell, 155, 1119, 10.1016/j.cell.2013.10.041 · DOI · Paper page
- Helman, 2016, p16 Ink4a-induced senescence of pancreatic beta cells enhances insulin secretion, Nat. Med., 22, 412, 10.1038/nm.4054 · DOI · Paper page
- Campisi, 1997, The biology of replicative senescence, Eur. J. Cancer Part A., 33, 703, 10.1016/S0959-8049(96)00058-5 · DOI
- Hayflick, 1965, The limited in vitro lifetime of human diploid cell strains, Exp. Cell Res., 37, 614, 10.1016/0014-4827(65)90211-9 · DOI · Paper page
- Kuilman, 2010, The essence of senescence, Genes Dev., 24, 2463, 10.1101/gad.1971610 · DOI · Paper page
- Dimri, 1995, A biomarker that identifies senescent human cells in culture and in aging skin in vivo, Proc. Natl. Acad. Sci. U.S.A., 92, 9363, 10.1073/pnas.92.20.9363 · DOI · Paper page
- Freund, 2012, Lamin B1 loss is a senescence-associated biomarker, Mol. Biol. Cell, 23, 2066, 10.1091/mbc.e11-10-0884 · DOI · Paper page
- Shimi, 2011, The role of nuclear lamin B1 in cell proliferation and senescence, Genes Dev., 25, 2579, 10.1101/gad.179515.111 · DOI · Paper page
- Von Zglinicki, 1995, Lipofuscin accumulation and ageing of fibroblasts, Gerontology, 41, 95, 10.1159/000213728 · DOI
- Kirkland, 2017, Cellular senescence: a translational perspective, EBioMedicine, 21, 21, 10.1016/j.ebiom.2017.04.013 · DOI · Paper page
- Wang, 1995, Senescent human fibroblasts resist programmed cell death, and failure to suppress bcl2 is involved, Canc. Res., 55
- Childs, 2014, Senescence and apoptosis: dueling or complementary cell fates?, EMBO Rep., 15, 1139, 10.15252/embr.201439245 · DOI · Paper page
- Mayorga, 2004, Bcl-2 is a key factor for cardiac fibroblast resistance to programmed cell death, J. Biol. Chem., 279, 34882, 10.1074/jbc.M404616200 · DOI
- Seluanov, 2001, Change of the death pathway in senescent human fibroblasts in response to DNA damage is caused by an inability to stabilize p53, Mol. Cell Biol., 21, 1552, 10.1128/MCB.21.5.1552-1564.2001 · DOI · Paper page
- Chaturvedi, 1999, Apoptosis in proliferating, senescent, and immortalized keratinocytes, J. Biol. Chem., 274, 23358, 10.1074/jbc.274.33.23358 · DOI
- Kirkland, 2017, The clinical potential of senolytic drugs, J. Am. Geriatr. Soc., 65, 2297, 10.1111/jgs.14969 · DOI · Paper page
- Peters, 2009, Reactive oxygen intermediate-induced pathomechanisms contribute to immunosenescence, chronic inflammation and autoimmunity, Mech. Ageing Dev., 130, 564, 10.1016/j.mad.2009.07.003 · DOI
- De Martinis, 2005, Inflamm-ageing and lifelong antigenic load as major determinants of ageing rate and longevity, FEBS Lett., 579, 2035, 10.1016/j.febslet.2005.02.055 · DOI
- Cevenini, 2013, Inflamm-ageing, Curr. Opin. Clin. Nutr. Metab. Care, 16, 14
- Prata, 2018, Senescent cell clearance by the immune system: emerging therapeutic opportunities, Semin. Immunol., 40, 10.1016/j.smim.2019.04.003 · DOI · Paper page
- Xu, 2017, Transplanted senescent cells induce an osteoarthritis-like condition in mice, J. Gerontol. A. Biol. Sci. Med. Sci., 72, 780
- Childs, 2016, Senescent intimal foam cells are deleterious at all stages of atherosclerosis, Science (80-. ), 354, 472, 10.1126/science.aaf6659 · DOI · Paper page
- Farr, 2017, Targeting cellular senescence prevents age-related bone loss in mice, Nat. Med., 23, 1072, 10.1038/nm.4385 · DOI · Paper page
- Krtolica, 2001, Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging, Proc. Natl. Acad. Sci. U.S.A., 98, 12072, 10.1073/pnas.211053698 · DOI · Paper page
- Minamino, 2009, A crucial role for adipose tissue p53 in the regulation of insulin resistance, Nat. Med., 15, 1082, 10.1038/nm.2014 · DOI · Paper page
- Tominaga, 2015, The emerging role of senescent cells in tissue homeostasis and pathophysiology, Pathobiol. Aging Age-Related Dis., 5, 27743, 10.3402/pba.v5.27743 · DOI
- Libby, 2009, Inflammation in atherosclerosis. From pathophysiology to practice, J. Am. Coll. Cardiol., 54, 2129, 10.1016/j.jacc.2009.09.009 · DOI · Paper page
- Coppé, 2010, The senescence-associated secretory phenotype: the dark side of tumor suppression, Annu. Rev. Pathol. Mech. Dis., 5, 99, 10.1146/annurev-pathol-121808-102144 · DOI · Paper page
- Lunyak, 2017, Mesenchymal stem cells secretory responses: senescence messaging secretome and immunomodulation perspective, Front. Genet., 8, 220, 10.3389/fgene.2017.00220 · DOI
- Xu, 2013, The role of exosomes and microRNAs in senescence and aging, Adv. Drug Deliv. Rev., 65, 368, 10.1016/j.addr.2012.07.010 · DOI
- Roberts, 1981, New class of transforming growth factors potentiated by epidermal growth factor: isolation from non-neoplastic tissues, Proc. Natl. Acad. Sci. U.S.A., 78, 5339, 10.1073/pnas.78.9.5339 · DOI
- Chien, 2011, Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity, Genes Dev., 25, 2125, 10.1101/gad.17276711 · DOI · Paper page
- Orjalo, 2009, Cell surface-bound IL-1α is an upstream regulator of the senescence-associated IL-6/IL-8 cytokine network, Proc. Natl. Acad. Sci. U.S.A., 106, 17031, 10.1073/pnas.0905299106 · DOI · Paper page
- Wedel, 1995, The C/EBP family of transcription factors, Immunobiology, 193, 171, 10.1016/S0171-2985(11)80541-3 · DOI
- Schreck, 1991, Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-κB transcription factor and HIV-1, EMBO J., 10, 2247, 10.1002/j.1460-2075.1991.tb07761.x · DOI
- Halvey, 2007, Selective oxidative stress in cell nuclei by nuclear-targeted D-amino acid oxidase, Antioxidants Redox Signal., 9, 807, 10.1089/ars.2007.1526 · DOI
- Lu, 2005, Oxidative stress augments the production of matrix Metalloproteinase-1, cyclooxygenase-2, and prostaglandin E 2 through enhancement of NF-κB activity in lipopolysaccharide-activated human primary monocytes, J. Immunol., 175, 5423, 10.4049/jimmunol.175.8.5423 · DOI
- Vanden Berghe, 1998, p38 and extracellular signal-regulated kinase mitogen-activated protein kinase pathways are required for nuclear factor-κB p65 transactivation mediated by tumor necrosis factor, J. Biol. Chem., 273, 3285, 10.1074/jbc.273.6.3285 · DOI
- Chong, 2018, CD 36 initiates the secretory phenotype during the establishment of cellular senescence, EMBO Rep., 19, 10.15252/embr.201745274 · DOI
- Wang, 2014, Protein kinase D1 is essential for Ras-induced senescence and tumor suppression by regulating senescence-associated inflammation, Proc. Natl. Acad. Sci. U.S.A., 111, 7683, 10.1073/pnas.1310972111 · DOI
- Saha, 2020, An Overview of Nrf2 signaling pathway and its role in inflammation, Molecules, 25, 5474, 10.3390/molecules25225474 · DOI
- Nguyen, 2004, The pathways and molecular mechanisms regulating Nrf2 activation in response to chemical stress, Free Radic. Biol. Med., 37, 433, 10.1016/j.freeradbiomed.2004.04.033 · DOI
- Lefaki, 2017, Redox regulation of proteasome function, Redox Biol, 13, 452, 10.1016/j.redox.2017.07.005 · DOI
- Furukawa, 2005, BTB protein Keap1 targets antioxidant transcription factor Nrf2 for ubiquitination by the cullin 3-Roc1 Ligase, Mol. Cell Biol., 25, 162, 10.1128/MCB.25.1.162-171.2005 · DOI
- Ahmed, 2017, Nrf2 signaling pathway: pivotal roles in inflammation, Biochim. Biophys. Acta (BBA) - Mol. Basis Dis., 1863, 585, 10.1016/j.bbadis.2016.11.005 · DOI · Paper page
- Ciais, 2004, Destabilization of vascular endothelial growth factor mRNA by the zinc-finger protein TIS11b, Oncogene, 23, 8673, 10.1038/sj.onc.1207939 · DOI
- Duhé, 2013, Redox regulation of Janus kinase, JAK-STAT, 2, 10.4161/jkst.26141 · DOI
- Garbers, 2013, An lnterleukin-6 receptor-dependent molecular switch mediates signal transduction of the IL-27 cytokine subunit p28 (IL-30) via a gp130 protein receptor homodimer, J. Biol. Chem., 288, 4346, 10.1074/jbc.M112.432955 · DOI
- Lopes, 1997, p53-dependent induction of apoptosis by proteasome inhibitors, J. Biol. Chem., 272, 12893, 10.1074/jbc.272.20.12893 · DOI
- Kim, 2018, Mitochondrial peptides modulate mitochondrial function during cellular senescence, Aging (Albany. NY), 10, 1239, 10.18632/aging.101463 · DOI
- Kim, 2019, Senotherapeutics: emerging strategy for healthy aging and age-related disease, BMB Rep, 52, 47, 10.5483/BMBRep.2019.52.1.293 · DOI
- von Kobbe, 2019, Targeting senescent cells: approaches, opportunities, challenges, Aging (Albany. NY), 11, 12844, 10.18632/aging.102557 · DOI
- Yang, 1999, Fully human anti-interleukin-8 monoclonal antibodies: potential therapeutics for the treatment of inflammatory disease states, J. Leukoc. Biol., 66, 401, 10.1002/jlb.66.3.401 · DOI
- Schafer, 2017, Cellular senescence: implications for metabolic disease, Mol. Cell. Endocrinol., 455, 93, 10.1016/j.mce.2016.08.047 · DOI
- Wiley, 2019, Secretion of leukotrienes by senescent lung fibroblasts promotes pulmonary fibrosis, JCI Insight, 4, 10.1172/jci.insight.130056 · DOI
- Ballou, 2008, Rapamycin and mTOR kinase inhibitors, J. Chem. Biol., 1, 27, 10.1007/s12154-008-0003-5 · DOI
- Li, 2014, Rapamycin: one drug, many effects, Cell Metabol., 19, 373, 10.1016/j.cmet.2014.01.001 · DOI · Paper page
- Wang, 2017, Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism, Aging Cell, 16, 564, 10.1111/acel.12587 · DOI · Paper page
- Bitto, 2016, Transient rapamycin treatment can increase lifespan and healthspan in middle-aged mice, Elife, 5, 10.7554/eLife.16351 · DOI · Paper page
- Szaniawski, 2020, Senotherapeutics and HIV-1 persistence, Curr. HIV AIDS Rep., 17, 219, 10.1007/s11904-020-00496-0 · DOI
- Kopp, 1998, Resveratrol, a phytoestrogen found in red wine. A possible explanation for the conundrum of the “French paradox”?, Eur. J. Endocrinol., 138, 619, 10.1530/eje.0.1380619 · DOI
- Frankel, 1993, Inhibition of human LDL oxidation by resveratrol, Lancet, 341, 1103, 10.1016/0140-6736(93)92472-6 · DOI
- Menicacci, 2017, Chronic resveratrol treatment inhibits MRC5 fibroblast SASP-related protumoral effects on melanoma cells, J. Gerontol. Ser. A., 72, 1187, 10.1093/gerona/glw336 · DOI
- Menicacci, 2019, Chronic resveratrol treatment reduces the pro-angiogenic effect of human fibroblast “senescent-associated secretory phenotype” on endothelial colony-forming cells: the role of IL8, Journals Gerontol. Ser. A., 74, 625, 10.1093/gerona/gly175 · DOI
- Liu, 2018, Resveratrol reduces senescence-associated secretory phenotype by SIRT1/NF-κB pathway in gut of the annual fish Nothobranchius guentheri, Fish Shellfish Immunol., 80, 473, 10.1016/j.fsi.2018.06.027 · DOI
- Xu, 2018, Inhibition of NF-κB signaling pathway by resveratrol improves spinal cord injury, Front. Neurosci., 12, 690, 10.3389/fnins.2018.00690 · DOI
- Ginés, 2017, Protective effect of resveratrol against inflammation, oxidative stress and apoptosis in pancreas of aged SAMP8 mice, Exp. Gerontol., 90, 61, 10.1016/j.exger.2017.01.021 · DOI
- Rha, 2019, Antioxidative, anti-inflammatory, and anticancer effects of purified flavonol glycosides and aglycones in green tea, Antioxidants, 8, 278, 10.3390/antiox8080278 · DOI
- Lee, 2019, Sirtuin signaling in cellular senescence and aging, BMB Rep, 52, 24, 10.5483/BMBRep.2019.52.1.290 · DOI
- Lee, 2020, Metabolite profiling of rambutan (Nephelium lappaceum L.) seeds using UPLC-qTOF-MS/MS and senomorphic effects in aged human dermal fibroblasts, Nutrients, 12, 1430, 10.3390/nu12051430 · DOI
- Niu, 2013, The phytochemical, EGCG, extends lifespan by reducing liver and kidney function damage and improving age-associated inflammation and oxidative stress in healthy rats, Aging Cell, 12, 1041, 10.1111/acel.12133 · DOI
- Sharma, 2017, Consumption of green tea epigallocatechin-3-gallate enhances systemic immune response, antioxidative capacity and HPA axis functions in aged male swiss albino mice, Biogerontology, 18, 367, 10.1007/s10522-017-9696-6 · DOI
- Farkhondeh, 2018, The protective effects of green tea catechins in the management of neurodegenerative diseases: a review, Curr. Drug Discov. Technol., 16, 57, 10.2174/1570163815666180219115453 · DOI
- Kumar, 2019, Epigallocatechin gallate suppresses premature senescence of preadipocytes by inhibition of PI3K/Akt/mTOR pathway and induces senescent cell death by regulation of Bax/Bcl-2 pathway, Biogerontology, 20, 171, 10.1007/s10522-018-9785-1 · DOI
- Han, 2012, Preventive effects of epigallocatechin-3- O -gallate against replicative senescence associated with p53 acetylation in human dermal fibroblasts, Oxid. Med. Cell. Longev., 2012, 10.1155/2012/850684 · DOI
- Shin, 2016, Epigallocatechin-3-gallate prevents oxidative stress-induced cellular senescence in human mesenchymal stem cells via Nrf2, Int. J. Mol. Med., 38, 1075, 10.3892/ijmm.2016.2694 · DOI
- Lilja, 2020, Epigallocatechin gallate effectively affects senescence and anti-SASP via SIRT3 in 3T3-L1 preadipocytes in comparison with other bioactive substances, Oxid. Med. Cell. Longev., 2020, 10.1155/2020/4793125 · DOI
- Kasai, 2020, Regulation of Nrf2 by mitochondrial reactive oxygen species in physiology and pathology, Biomolecules, 10, 10.3390/biom10020320 · DOI
- Moiseeva, 2013, Metformin inhibits the senescence-associated secretory phenotype by interfering with IKK/NF-κB activation, Aging Cell, 12, 489, 10.1111/acel.12075 · DOI · Paper page
- Barzilai, 2017, Targeting aging with metformin (TAME), Innov. Aging., 1, 10.1093/geroni/igx004.2682 · DOI · Paper page
- Cabreiro, 2013, Metformin retards aging in C. elegans by altering microbial folate and methionine metabolism, Cell, 153, 228, 10.1016/j.cell.2013.02.035 · DOI · Paper page
- Harrison, 2016, Ruxolitinib is effective in patients with intermediate-1 risk myelofibrosis: a summary of recent evidence, Leuk. Lymphoma, 57, 2259, 10.1080/10428194.2016.1195501 · DOI
- Gensler, 2013, Glucocorticoids: complications to anticipate and prevent, The Neurohospitalist, 3, 92, 10.1177/1941874412458678 · DOI · Paper page
- Laberge, 2012, Glucocorticoids suppress selected components of the senescence-associated secretory phenotype, Aging Cell, 11, 569, 10.1111/j.1474-9726.2012.00818.x · DOI · Paper page
- Fuhrmann-Stroissnigg, 2017, Identification of HSP90 inhibitors as a novel class of senolytics, Nat. Commun., 8, 10.1038/s41467-017-00314-z · DOI · Paper page
- Banin, 1998, Enhanced phosphorylation of p53 by ATM in response to DNA damage, Science (80-, 281, 1674, 10.1126/science.281.5383.1674 · DOI · Paper page
- Yamaoka, 1998, Complementation cloning of NEMO, a component of the IκB kinase complex essential for NF-κB activation, Cell, 93, 1231, 10.1016/S0092-8674(00)81466-X · DOI
- Bae, 2019, Embryonic stem cell-derived mmu-miR-291a-3p inhibits cellular senescence in human dermal fibroblasts through the TGF-β receptor 2 pathway, J. Gerontol. - Ser. A Biol. Sci. Med. Sci., 74, 1359, 10.1093/gerona/gly208 · DOI
- Zhu, 2016, Identification of a novel senolytic agent, navitoclax, targeting the Bcl-2 family of anti-apoptotic factors, Aging Cell, 15, 428, 10.1111/acel.12445 · DOI · Paper page
- Morand, 1998, Plasma metabolites of quercetin and their antioxidant properties, Am. J. Physiol. Regul. Integr. Comp. Physiol., 275, 10.1152/ajpregu.1998.275.1.R212 · DOI
- Hashemzaei, 2017, Anticancer and apoptosis-inducing effects of quercetin in vitro and in vivo, Oncol. Rep., 38, 819, 10.3892/or.2017.5766 · DOI
- Chondrogianni, 2010, Anti-ageing and rejuvenating effects of quercetin, Exp. Gerontol., 45, 763, 10.1016/j.exger.2010.07.001 · DOI
- Kampkötter, 2008, Increase of stress resistance and lifespan of Caenorhabditis elegans by quercetin, Comp. Biochem. Physiol. B Biochem. Mol. Biol., 149, 314, 10.1016/j.cbpb.2007.10.004 · DOI
- Shao, 2021, Senolytic agent Quercetin ameliorates intervertebral disc degeneration via the Nrf2/NF-κB axis, Osteoarthritis Cartilage, 29, 413, 10.1016/j.joca.2020.11.006 · DOI
- Wang, 2016, The biological activities, chemical stability, metabolism and delivery systems of quercetin: a review, Trends Food Sci. Technol., 56, 21, 10.1016/j.tifs.2016.07.004 · DOI
- Naeimi, 2017, Antioxidant properties of the flavonoid fisetin: an updated review of in vivo and in vitro studies, Trends Food Sci. Technol., 70, 34, 10.1016/j.tifs.2017.10.003 · DOI
- Gutiérrez-Venegas, 2014, Anti-inflammatory activity of fisetin in human gingival fibroblasts treated with lipopolysaccharide, J. Asian Nat. Prod. Res., 16, 1009, 10.1080/10286020.2014.932351 · DOI
- Sandireddy, 2016, Fisetin imparts Neuroprotection in experimental diabetic neuropathy by modulating Nrf2 and NF-κB pathways, Cell. Mol. Neurobiol., 36, 883, 10.1007/s10571-015-0272-9 · DOI
- Yousefzadeh, 2018, Fisetin is a senotherapeutic that extends health and lifespan, EBioMedicine, 36, 18, 10.1016/j.ebiom.2018.09.015 · DOI · Paper page
- Zhang, 2018, Oxidation resistance 1 is a novel senolytic target, Aging Cell, 17, 10.1111/acel.12780 · DOI · Paper page
- Kim, 2014, Piperlongumine treatment inactivates peroxiredoxin 4, exacerbates endoplasmic reticulum stress, and preferentially kills high-grade glioma cells, Neuro Oncol., 16, 1354, 10.1093/neuonc/nou088 · DOI
- Qian, 2016, Implication of differential peroxiredoxin 4 expression with age in ovaries of mouse and human for ovarian aging, Curr. Mol. Med., 16, 243, 10.2174/1566524016666160225151647 · DOI
- Liang, 2020, Peroxiredoxin 4 protects against ovarian ageing by ameliorating d-galactose-induced oxidative damage in mice, Cell Death Dis., 11, 1, 10.1038/s41419-020-03253-8 · DOI
- Kim, 2018, Piperlongumine inhibits neuroinflammation via regulating NF-κB signaling pathways in lipopolysaccharide-stimulated BV2 microglia cells, J. Pharmacol. Sci., 137, 195, 10.1016/j.jphs.2018.06.004 · DOI
- Go, 2018, Piperlongumine decreases cognitive impairment and improves hippocampal function in aged mice, Int. J. Mol. Med., 42, 1875
- Liu, 2018, Piperlongumine restores the balance of autophagy and apoptosis by increasing BCL2 phosphorylation in rotenone-induced Parkinson disease models, Autophagy, 14, 845, 10.1080/15548627.2017.1390636 · DOI
- Kocaadam, 2017, Curcumin, an active component of turmeric (Curcuma longa), and its effects on health, Crit. Rev. Food Sci. Nutr., 57, 2889, 10.1080/10408398.2015.1077195 · DOI
- Chandrashekara, 2014, Curcumin enhances parental reproductive lifespan and progeny viability in Drosophila melanogaster, Age, 36, 10.1007/s11357-014-9702-8 · DOI
- Liao, 2011, Curcumin-mediated lifespan extension in Caenorhabditis elegans, Mech. Ageing Dev., 132, 480, 10.1016/j.mad.2011.07.008 · DOI
- Balogun, 2003, Curcumin activates the haem oxygenase-1 gene via regulation of Nrf2 and the antioxidant-responsive element, Biochem. J., 371, 887, 10.1042/bj20021619 · DOI
- Das, 2018, Curcumin modulates glycolytic metabolism and inflammatory cytokines via Nrf 2 in dalton's lymphoma ascites cells in vivo, anticancer, Agents Med. Chem., 18, 1779
- Fattori, 2015, Curcumin inhibits superoxide anion-induced pain-like behavior and leukocyte recruitment by increasing Nrf2 expression and reducing NF-κB activation, Inflamm. Res., 64, 993, 10.1007/s00011-015-0885-y · DOI
- Cherif, 2019, Curcumin and o-vanillin exhibit evidence of senolytic activity in human IVD cells in vitro, J. Clin. Med., 8, 433, 10.3390/jcm8040433 · DOI
- Boyanapalli, 2014, Nrf2 knockout attenuates the anti-inflammatory effects of phenethyl isothiocyanate and curcumin, Chem. Res. Toxicol., 27, 2036, 10.1021/tx500234h · DOI
- Li, 2019, The curcumin analog EF24 is a novel senolytic agent, Aging (Albany. NY), 11, 771, 10.18632/aging.101787 · DOI · Paper page
- Purpura, 2018, Analysis of different innovative formulations of curcumin for improved relative oral bioavailability in human subjects, Eur. J. Nutr., 57, 929, 10.1007/s00394-016-1376-9 · DOI
- He, 2018, Bioactivities of EF24, a novel curcumin analog: a review, Front. Oncol., 8, 614, 10.3389/fonc.2018.00614 · DOI
- Li, 2009, Characterization of dasatinib and its structural analogs as CYP3A4 mechanism-based inactivators and the proposed bioactivation pathways, Drug Metab. Dispos., 37, 1242, 10.1124/dmd.108.025932 · DOI
- Montero, 2011, Inhibition of Src family kinases and receptor tyrosine kinases by dasatinib: possible combinations in solid tumors, Clin. Canc. Res., 17, 5546, 10.1158/1078-0432.CCR-10-2616 · DOI · Paper page
- Kovacovicova, 2018, Senolytic cocktail Dasatinib+Quercetin (D+Q) does not enhance the efficacy of senescence-inducing chemotherapy in liver cancer, Front. Oncol., 8, 459, 10.3389/fonc.2018.00459 · DOI
- Tullius, 2011, Kidney allocation and the aging immune response, N. Engl. J. Med., 364, 1369, 10.1056/NEJMc1103007 · DOI
- Oberhuber, 2015, CD11c+ dendritic cells accelerate the rejection of older cardiac transplants via interleukin-17a, Circulation, 132, 122, 10.1161/CIRCULATIONAHA.114.014917 · DOI
- Iske, 2020, Senolytics prevent mt-DNA-induced inflammation and promote the survival of aged organs following transplantation, Nat. Commun., 11, 10.1038/s41467-020-18039-x · DOI · Paper page
- Tse, 2008, ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor, Canc. Res., 68, 3421, 10.1158/0008-5472.CAN-07-5836 · DOI · Paper page
- Chang, 2016, Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice, Nat. Med., 22, 78, 10.1038/nm.4010 · DOI · Paper page
- Yang, 2020, Navitoclax (ABT263) reduces inflammation and promotes chondrogenic phenotype by clearing senescent osteoarthritic chondrocytes in osteoarthritis, Aging (Albany. NY), 12, 12750, 10.18632/aging.103177 · DOI
- Rudin, 2012, Phase II study of single-agent navitoclax (ABT-263) and biomarker correlates in patients with relapsed small cell lung cancer, Clin. Canc. Res., 18, 3163, 10.1158/1078-0432.CCR-11-3090 · DOI
- Oltersdorf, 2005, An inhibitor of Bcl-2 family proteins induces regression of solid tumours, Nature, 435, 677, 10.1038/nature03579 · DOI
- Moncsek, 2018, Targeting senescent cholangiocytes and activated fibroblasts with B-cell lymphoma-extra large inhibitors ameliorates fibrosis in multidrug resistance 2 gene knockout (Mdr2−/−) mice, Hepatology, 67, 247, 10.1002/hep.29464 · DOI · Paper page
- Jeon, 2017, Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment, Nat. Med., 23, 775, 10.1038/nm.4324 · DOI · Paper page
- Dolgin, 2020, Send in the senolytics, Nat. Biotechnol., 38, 10.1038/s41587-020-00750-1 · DOI
- Chauhan, 2012, A small molecule inhibitor of ubiquitin-specific protease-7 induces apoptosis in multiple myeloma cells and overcomes Bortezomib resistance, Canc. Cell, 22, 345, 10.1016/j.ccr.2012.08.007 · DOI · Paper page
- He, 2020, Inhibition of USP7 activity selectively eliminates senescent cells in part via restoration of p53 activity, Aging Cell, 19, 10.1111/acel.13117 · DOI
- Li, 2004, A dynamic role of HAUSP in the p53-Mdm2 pathway, Mol. Cell., 13, 879, 10.1016/S1097-2765(04)00157-1 · DOI · Paper page
- Bourgeois, 2018, Regulation of cellular senescence via the FOXO4-p53 axis, FEBS Lett., 592, 2083, 10.1002/1873-3468.13057 · DOI
- Cheng, 2015, Panobinostat, a pan-histone deacetylase inhibitor: Rationale for and application to treatment of multiple myeloma, Drugs Today, 51, 491, 10.1358/dot.2015.51.8.2362311 · DOI
- Rada-Iglesias, 2007, Butyrate mediates decrease of histone acetylation centered on transcription start sites and down-regulation of associated genes, Genome Res., 17, 708, 10.1101/gr.5540007 · DOI
- Duan, 2005, Histone deacetylase inhibitors down-regulate bcl-2 expression and induce apoptosis in t(14;18) lymphomas, Mol. Cell Biol., 25, 1608, 10.1128/MCB.25.5.1608-1619.2005 · DOI
- Hubackova, 2019, Selective elimination of senescent cells by mitochondrial targeting is regulated by ANT2, Cell Death Differ., 26, 276, 10.1038/s41418-018-0118-3 · DOI
- Harwood, 2007, A critical review of the data related to the safety of quercetin and lack of evidence of in vivo toxicity, including lack of genotoxic/carcinogenic properties, Food Chem. Toxicol., 45, 2179, 10.1016/j.fct.2007.05.015 · DOI
- Grosse, 2020, Defined p16High senescent cell types are indispensable for mouse healthspan, Cell Metabol., 32, 87, 10.1016/j.cmet.2020.05.002 · DOI · Paper page
- Martin, 2021, Elimination of senescent endothelial cells: good or bad idea?, Trends Cell Biol., 10.1016/j.tcb.2021.02.009 · DOI
- Wiley, 2021, Oxylipin biosynthesis reinforces cellular senescence and allows detection of senolysis, Cell Metabol., 10.1016/j.cmet.2021.03.008 · DOI · Paper page
- Fossel, 2018, Cell senescence, telomerase, and senolytic therapy, OBM Geriatr, 3, 10.21926/obm.geriatr.1901034 · DOI
- Eggler, 2008, Molecular mechanisms of natural products in chemoprevention: induction of cytoprotective enzymes by Nrf2, Mol. Nutr. Food Res., 52
- Papaevgeniou, 2016, 18α-Glycyrrhetinic acid proteasome activator decelerates aging and Alzheimer's disease progression in caenorhabditis elegans and neuronal cultures, Antioxidants Redox Signal., 25, 855, 10.1089/ars.2015.6494 · DOI
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Metadata
- Authors
- Lagoumtzi, S. M., & Chondrogianni, N.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2021-08
- Volume
- 171
- Pages
- 169-190
- ISSN
- 0891-5849
- Cited by
- 279
- References
- 111
- Language
- en
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