The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Metabolic remodeling in cancer and senescence and its therapeutic implications
Abstract
Cellular metabolism is a flexible and plastic network that often dictates physiological and pathological states of the cell, including differentiation, cancer, and aging. Recent advances in cancer metabolism represent a tremendous opportunity to treat cancer by targeting its altered metabolism. Interestingly, despite their stable growth arrest, senescent cells - a critical component of the aging process - undergo metabolic changes similar to cancer metabolism. A deeper understanding of the similarities and differences between these disparate pathological conditions will help identify which metabolic reprogramming is most relevant to the therapeutic liabilities of senescence. Here, we compare and contrast cancer and senescence metabolism and discuss how metabolic therapies can be established as a new modality of senotherapy for healthy aging.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The future of senotherapy may lie in precision reprogramming through the synergistic modulation of immunity, protein degradation, and metabolism.
“As discussed, the future of senotherapy may lie in precision reprogramming through the synergistic modulation of immunity, protein degradation, and metabolism141,142.”
From Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming (2026) · cites this paper as [141]
Citations
Cites
Hallmarks of Cancer: New Dimensions
Hanahan, D. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-1059 · Cited by 9,887
Hallmarks of aging: An expanding universe
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2023) · Cell · doi:10.1016/j.cell.2022.11.001 · Cited by 6,549
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670
Cellular Senescence: Defining a Path Forward
Gorgoulis, V., Adams, P. D., Alimonti, A., Bennett, D. C., Bischof, O., Bishop, C., Campisi, J., Collado, M., Evangelou, K., Ferbeyre, G., et al. (2019) · Cell · doi:10.1016/j.cell.2019.10.005 · Cited by 3,225
Fundamentals of Cancer Metabolism
DeBerardinis, R. J., & Chandel, N. S. (2016) · Science Advances · doi:10.1126/sciadv.1600200 · Cited by 3,013
Naturally occurring p16Ink4a-positive cells shorten healthy lifespan
Baker, D. J., Childs, B. G., Durik, M., Wijers, M. E., Sieben, C. J., Zhong, J., A. Saltness, R., Jeganathan, K. B., Verzosa, G. C., Pezeshki, A., et al. (2016) · Nature · doi:10.1038/nature16932 · Cited by 2,876
Metabolic reprogramming and cancer progression
Faubert, B., Solmonson, A., & DeBerardinis, R. J. (2020) · Science · doi:10.1126/science.aaw5473 · Cited by 2,740
mTOR at the nexus of nutrition, growth, ageing and disease
Liu, G. Y., & Sabatini, D. M. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0199-y · Cited by 2,737
The Achilles' heel of senescent cells: from transcriptome to senolytic drugs
Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., Palmer, A. K., Ikeno, Y., Hubbard, G. B., Lenburg, M., et al. (2015) · Aging Cell · doi:10.1111/acel.12344 · Cited by 2,584
Senolytics improve physical function and increase lifespan in old age
Xu, M., Pirtskhalava, T., Farr, J. N., Weigand, B. M., Palmer, A. K., Weivoda, M. M., Inman, C. L., Ogrodnik, M. B., Hachfeld, C. M., Fraser, D. G., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0092-9 · Cited by 2,287
Cellular senescence in ageing: from mechanisms to therapeutic opportunities
Di Micco, R., Krizhanovsky, V., Baker, D., & d’Adda di Fagagna, F. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-00314-w · Cited by 2,277
Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype
Wiley, C. D., Velarde, M. C., Lecot, P., Liu, S., Sarnoski, E. A., Freund, A., Shirakawa, K., Lim, H. W., Davis, S. S., Ramanathan, A., et al. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.11.011 · Cited by 1,275
Mechanisms and functions of cellular senescence
Herranz, N., & Gil, J. (2018) · Journal of Clinical Investigation · doi:10.1172/jci95148 · Cited by 1,232
Targeting cancer metabolism in the era of precision oncology
Stine, Z. E., Schug, Z. T., Salvino, J. M., & Dang, C. V. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-021-00339-6 · Cited by 1,189
Senescence and the SASP: many therapeutic avenues
Birch, J., & Gil, J. (2020) · Genes & Development · doi:10.1101/gad.343129.120 · Cited by 1,177
Laberge, R.-M., Sun, Y., Orjalo, A. V., Patil, C. K., Freund, A., Zhou, L., Curran, S. C., Davalos, A. R., Wilson-Edell, K. A., Liu, S., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3195 · Cited by 1,160
Cellular senescence and senolytics: the path to the clinic
Chaib, S., Tchkonia, T., & Kirkland, J. L. (2022) · Nature Medicine · doi:10.1038/s41591-022-01923-y · Cited by 1,134
Senolytic CAR T cells reverse senescence-associated pathologies
Amor, C., Feucht, J., Leibold, J., Ho, Y.-J., Zhu, C., Alonso-Curbelo, D., Mansilla-Soto, J., Boyer, J. A., Li, X., Giavridis, T., et al. (2020) · Nature · doi:10.1038/s41586-020-2403-9 · Cited by 1,098
Mitochondrial dysfunction in cell senescence and aging
Miwa, S., Kashyap, S., Chini, E., & von Zglinicki, T. (2022) · Journal of Clinical Investigation · doi:10.1172/jci158447 · Cited by 1,061
The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4.
Kang, C., Xu, Q., Martin, T. D., Li, M. Z., Demaria, M., Aron, L., Lu, T., Yankner, B. A., Campisi, J., & Elledge, S. J. (2015) · Science · doi:10.1126/science.aaa5612 · Cited by 982
Self-citationUnmasking Transcriptional Heterogeneity in Senescent Cells
Hernandez-Segura, A., de Jong, T. V., Melov, S., Guryev, V., Campisi, J., & Demaria, M. (2017) · Current Biology · doi:10.1016/j.cub.2017.07.033 · Cited by 972
The lysosome as a cellular centre for signalling, metabolism and quality control
Lawrence, R. E., & Zoncu, R. (2019) · Nature Cell Biology · doi:10.1038/s41556-018-0244-7 · Cited by 920
Unmasking senescence: context-dependent effects of SASP in cancer
Faget, D. V., Ren, Q., & Stewart, S. A. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0156-2 · Cited by 863
Senescence and cancer — role and therapeutic opportunities
Schmitt, C. A., Wang, B., & Demaria, M. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00668-4 · Cited by 794
mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype
Herranz, N., Gallage, S., Mellone, M., Wuestefeld, T., Klotz, S., Hanley, C. J., Raguz, S., Acosta, J. C., Innes, A. J., Banito, A., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3225 · Cited by 788
Autophagy mediates degradation of nuclear lamina
Dou, Z., Xu, C., Donahue, G., Shimi, T., Pan, J.-A., Zhu, J., Ivanov, A., Capell, B. C., Drake, A. M., Shah, P. P., et al. (2015) · Nature · doi:10.1038/nature15548 · Cited by 655
Cellular senescence: a key therapeutic target in aging and diseases
Zhang, L., Pitcher, L. E., Yousefzadeh, M. J., Niedernhofer, L. J., Robbins, P. D., & Zhu, Y. (2022) · Journal of Clinical Investigation · doi:10.1172/jci158450 · Cited by 631
Spatial Coupling of mTOR and Autophagy Augments Secretory Phenotypes
Narita, M., Young, A. R. J., Arakawa, S., Samarajiwa, S. A., Nakashima, T., Yoshida, S., Hong, S., Berry, L. S., Reichelt, S., Ferreira, M., et al. (2011) · Science · doi:10.1126/science.1205407 · Cited by 594
Excessive Cell Growth Causes Cytoplasm Dilution And Contributes to Senescence
Neurohr, G. E., Terry, R. L., Lengefeld, J., Bonney, M., Brittingham, G. P., Moretto, F., Miettinen, T. P., Vaites, L. P., Soares, L. M., Paulo, J. A., et al. (2019) · Cell · doi:10.1016/j.cell.2019.01.018 · Cited by 518
Nutrient acquisition strategies of mammalian cells
Palm, W., & Thompson, C. B. (2017) · Nature · doi:10.1038/nature22379 · Cited by 388
Cardiac glycosides are broad-spectrum senolytics
Guerrero, A., Herranz, N., Sun, B., Wagner, V., Gallage, S., Guiho, R., Wolter, K., Pombo, J., Irvine, E. E., Innes, A. J., et al. (2019) · Nature Metabolism · doi:10.1038/s42255-019-0122-z · Cited by 359
The flavonoid procyanidin C1 has senotherapeutic activity and increases lifespan in mice
Xu, Q., Fu, Q., Li, Z., Liu, H., Wang, Y., Lin, X., He, R., Zhang, X., Ju, Z., Campisi, J., et al. (2021) · Nature Metabolism · doi:10.1038/s42255-021-00491-8 · Cited by 341
Coppé, J.-P., Patil, C. K., Rodier, F., Sun, Y., Muñoz, D. P., Goldstein, J., Nelson, P. S., Desprez, P.-Y., & Campisi, J. (2008) · PLoS Biology · doi:10.1371/journal.pbio.0060301 · Cited by 302
Slow TCA flux and ATP production in primary solid tumours but not metastases
Bartman, C. R., Weilandt, D. R., Shen, Y., Lee, W. D., Han, Y., TeSlaa, T., Jankowski, C. S. R., Samarah, L., Park, N. R., da Silva-Diz, V., et al. (2023) · Nature · doi:10.1038/s41586-022-05661-6 · Cited by 299
Flagged first, then by citations
Research works printed but not linked: 86
- Saxton, 2017, mTOR signaling in growth, metabolism, and disease, Cell, 168, 960, 10.1016/j.cell.2017.02.004 · DOI · Paper page
- Fendt, 2020, Targeting metabolic plasticity and flexibility dynamics for cancer therapy, Cancer Discov., 10, 1797, 10.1158/2159-8290.CD-20-0844 · DOI
- Martinez-Reyes, 2021, Cancer metabolism: looking forward, Nat. Rev. Cancer, 21, 669, 10.1038/s41568-021-00378-6 · DOI
- Mutlu, 2021, Lipid metabolism and lipid signals in aging and longevity, Dev. Cell, 56, 1394, 10.1016/j.devcel.2021.03.034 · DOI
- Pavlova, 2022, The hallmarks of cancer metabolism: still emerging, Cell Metab., 34, 355, 10.1016/j.cmet.2022.01.007 · DOI · Paper page
- Finley, 2023, What is cancer metabolism?, Cell, 186, 1670, 10.1016/j.cell.2023.01.038 · DOI
- Moldakozhayev, 2023, Metabolism, homeostasis, and aging, Trends Endocrinol. Metab., 34, 158, 10.1016/j.tem.2023.01.003 · DOI
- Xiao, 2023, Emerging therapies in cancer metabolism, Cell Metab., 35, 1283, 10.1016/j.cmet.2023.07.006 · DOI
- Kim, 2019, Mechanisms and implications of metabolic heterogeneity in cancer, Cell Metab., 30, 434, 10.1016/j.cmet.2019.08.013 · DOI · Paper page
- Zhu, 2019, Metabolic regulation of cell growth and proliferation, Nat. Rev. Mol. Cell Biol., 20, 436, 10.1038/s41580-019-0123-5 · DOI
- Hornburg, 2023, Dynamic lipidome alterations associated with human health, disease and ageing, Nat. Metab., 5, 1578, 10.1038/s42255-023-00880-1 · DOI
- Hanahan, 2011, Hallmarks of cancer: the next generation, Cell, 144, 646, 10.1016/j.cell.2011.02.013 · DOI · Paper page
- Calcinotto, 2019, Cellular senescence: aging, cancer, and injury, Physiol. Rev., 99, 1047, 10.1152/physrev.00020.2018 · 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
- Ring, 2022, The role of senescence in cellular plasticity: lessons from regeneration and development and implications for age-related diseases, Dev. Cell, 57, 1083, 10.1016/j.devcel.2022.04.005 · DOI
- Hernandez-Segura, 2018, Hallmarks of cellular senescence, Trends Cell Biol., 28, 436, 10.1016/j.tcb.2018.02.001 · DOI · Paper page
- Lanz, 2022, Increasing cell size remodels the proteome and promotes senescence, Mol. Cell, 82, 3255, 10.1016/j.molcel.2022.07.017 · DOI
- Crozier, 2023, CDK4/6 inhibitor-mediated cell overgrowth triggers osmotic and replication stress to promote senescence, Mol. Cell, 83, 4062, 10.1016/j.molcel.2023.10.016 · DOI
- Manohar, 2023, Genome homeostasis defects drive enlarged cells into senescence, Mol. Cell, 83, 4032, 10.1016/j.molcel.2023.10.018 · DOI
- Wiley, 2016, From ancient pathways to aging cells – connecting metabolism and cellular senescence, Cell Metab., 23, 1013, 10.1016/j.cmet.2016.05.010 · DOI · Paper page
- Wiley, 2021, The metabolic roots of senescence: mechanisms and opportunities for intervention, Nat. Metab., 3, 1290, 10.1038/s42255-021-00483-8 · DOI · Paper page
- Carroll, 2017, Persistent mTORC1 signaling in cell senescence results from defects in amino acid and growth factor sensing, J. Cell Biol., 216, 1949, 10.1083/jcb.201610113 · DOI
- Rabanal-Ruiz, 2021, mTORC1 activity is supported by spatial association with focal adhesions, J. Cell Biol., 220, 10.1083/jcb.202004010 · DOI
- Roh, 2023, Lysosomal control of senescence and inflammation through cholesterol partitioning, Nat. Metab., 5, 398, 10.1038/s42255-023-00747-5 · DOI
- Kang, 2019, Senolytics and senostatics: a two-pronged approach to target cellular senescence for delaying aging and age-related diseases, Mol. Cells, 42, 821
- van Deursen, 2019, Senolytic therapies for healthy longevity, Science, 364, 636, 10.1126/science.aaw1299 · DOI · Paper page
- Camell, 2021, Senolytics reduce coronavirus-related mortality in old mice, Science, 373, 10.1126/science.abe4832 · DOI · Paper page
- Johmura, 2021, Senolysis by glutaminolysis inhibition ameliorates various age-associated disorders, Science, 371, 265, 10.1126/science.abb5916 · DOI · Paper page
- Kim, 2022, A focused natural compound screen reveals senolytic and senostatic effects of Isatis tinctoria, Anim. Cells Syst. (Seoul), 26, 310, 10.1080/19768354.2022.2143895 · DOI
- Amor, 2023, Prophylactic and long-lasting efficacy of senolytic CAR T cells against age-related metabolic dysfunction, Nat. Aging
- D’Ambrosio, 2023, Reshaping of the tumor microenvironment by cellular senescence: an opportunity for senotherapies, Dev. Cell, 58, 1007, 10.1016/j.devcel.2023.05.010 · DOI
- McHugh, 2023, COPI vesicle formation and N-myristoylation are targetable vulnerabilities of senescent cells, Nat. Cell Biol., 25, 1804, 10.1038/s41556-023-01287-6 · DOI
- Kim, 2023, The role of pyruvate metabolism in mitochondrial quality control and inflammation, Mol. Cells, 46, 259, 10.14348/molcells.2023.2128 · DOI
- DeBerardinis, 2020, We need to talk about the Warburg effect, Nat. Metab., 2, 127, 10.1038/s42255-020-0172-2 · DOI
- Thompson, 2023, A century of the Warburg effect, Nat. Metab., 5, 1840, 10.1038/s42255-023-00927-3 · DOI
- Wang, 2023, The Warburg effect: a signature of mitochondrial overload, Trends Cell Biol., 33, 1014, 10.1016/j.tcb.2023.03.013 · DOI
- Pavlova, 2016, The emerging hallmarks of cancer metabolism, Cell Metab., 23, 27, 10.1016/j.cmet.2015.12.006 · DOI · Paper page
- Feng, 2023, Nrf2 in TIME: the emerging role of nuclear factor erythroid 2-related factor 2 in the tumor immune microenvironment, Mol. Cells, 46, 142, 10.14348/molcells.2023.2183 · DOI
- Fedele, 2022, The epithelial-mesenchymal transition at the crossroads between metabolism and tumor progression, Int. J. Mol. Sci., 23, 800, 10.3390/ijms23020800 · DOI
- Liu, 2023, Lipid and glucose metabolism in senescence, Front. Nutr., 10
- Mycielska, 2022, Metabolic alterations in cellular senescence: the role of citrate in ageing and age-related disease, Int. J. Mol. Sci., 23, 3652, 10.3390/ijms23073652 · DOI
- Dou, 2023, PDK4-dependent hypercatabolism and lactate production of senescent cells promotes cancer malignancy, Nat. Metab., 5, 1887, 10.1038/s42255-023-00912-w · DOI
- Pachnis, 2022, In vivo isotope tracing reveals a requirement for the electron transport chain in glucose and glutamine metabolism by tumors, Sci. Adv., 8, 10.1126/sciadv.abn9550 · DOI
- Bartman, 2023, Metabolic pathway analysis using stable isotopes in patients with cancer, Nat. Rev. Cancer, 23, 863, 10.1038/s41568-023-00632-z · DOI
- Wang, 2021, Defueling the cancer: ATP synthase as an emerging target in cancer therapy, Mol. Ther. Oncol., 23, 82, 10.1016/j.omto.2021.08.015 · DOI
- Yao, 2019, Mitochondrial fusion supports increased oxidative phosphorylation during cell proliferation, Elife, 8, 10.7554/eLife.41351 · DOI
- Zacharioudakis, 2022, Modulating mitofusins to control mitochondrial function and signaling, Nat. Commun., 13, 3775, 10.1038/s41467-022-31324-1 · DOI
- Martini, 2023, Cellular senescence: all roads lead to mitochondria, FEBS J., 290, 1186, 10.1111/febs.16361 · DOI · Paper page
- Moiseeva, 2013, Metformin inhibits the senescence-associated secretory phenotype by interfering with IKK/NF-kappaB activation, Aging Cell, 12, 489, 10.1111/acel.12075 · DOI · Paper page
- Hoxhaj, 2020, The PI3K-AKT network at the interface of oncogenic signalling and cancer metabolism, Nat. Rev. Cancer, 20, 74, 10.1038/s41568-019-0216-7 · DOI · Paper page
- Lee, 2021, Coordinate regulation of the senescent state by selective autophagy, Dev. Cell, 56, 1512, 10.1016/j.devcel.2021.04.008 · DOI
- Fafian-Labora, 2019, FASN activity is important for the initial stages of the induction of senescence, Cell Death Dis., 10, 318, 10.1038/s41419-019-1550-0 · DOI
- Kuehnemann, 2023, Cholesterol drives inflammatory senescence, Nat. Metab., 5, 355, 10.1038/s42255-023-00758-2 · DOI
- Koundouros, 2020, Reprogramming of fatty acid metabolism in cancer, Br. J. Cancer, 122, 4, 10.1038/s41416-019-0650-z · DOI
- Carracedo, 2013, Cancer metabolism: fatty acid oxidation in the limelight, Nat. Rev. Cancer, 13, 227, 10.1038/nrc3483 · DOI
- Wiley, 2021, Oxylipin biosynthesis reinforces cellular senescence and allows detection of senolysis, Cell Metab., 33, 1124, 10.1016/j.cmet.2021.03.008 · DOI · Paper page
- Hannun, 2018, Sphingolipids and their metabolism in physiology and disease, Nat. Rev. Mol. Cell Biol., 19, 175, 10.1038/nrm.2017.107 · DOI
- Trayssac, 2018, Role of sphingolipids in senescence: implication in aging and age-related diseases, J. Clin. Invest., 128, 2702, 10.1172/JCI97949 · DOI
- Choudhury, 2022, Inhibition of glutaminolysis restores mitochondrial function in senescent stem cells, Cell Rep., 41, 10.1016/j.celrep.2022.111744 · DOI
- Ballabio, 2020, Lysosomes as dynamic regulators of cell and organismal homeostasis, Nat. Rev. Mol. Cell Biol., 21, 101, 10.1038/s41580-019-0185-4 · DOI · Paper page
- Shin, 2020, The lysosome at the intersection of cellular growth and destruction, Dev. Cell, 54, 226, 10.1016/j.devcel.2020.06.010 · DOI
- Poillet-Perez, 2019, Role of tumor and host autophagy in cancer metabolism, Genes Dev., 33, 610, 10.1101/gad.325514.119 · DOI
- Kim, 2021, Targeting the stress support network regulated by autophagy and senescence for cancer treatment, Adv. Cancer Res., 150, 75, 10.1016/bs.acr.2021.01.003 · DOI
- Chae, 2023, Transcription factor EB-mediated lysosomal function regulation for determining stem cell fate under metabolic stress, Mol. Cells, 46, 727, 10.14348/molcells.2023.0143 · DOI
- Cai, 2023, Lactate activates the mitochondrial electron transport chain independently of its metabolism, Mol. Cell, 83, 3904, 10.1016/j.molcel.2023.09.034 · DOI
- Zou, 2020, mTOR signaling pathway and mTOR inhibitors in cancer: progress and challenges, Cell Biosci., 10, 31, 10.1186/s13578-020-00396-1 · DOI
- Lee, 2020, Targeting MAPK signaling in cancer: mechanisms of drug resistance and sensitivity, Int. J. Mol. Sci., 21, 1102, 10.3390/ijms21031102 · DOI
- He, 2021, Targeting PI3K/Akt signal transduction for cancer therapy, Signal Transduct. Target. Ther., 6, 425, 10.1038/s41392-021-00828-5 · DOI
- Mossmann, 2018, mTOR signalling and cellular metabolism are mutual determinants in cancer, Nat. Rev. Cancer, 18, 744, 10.1038/s41568-018-0074-8 · DOI · Paper page
- Carroll, 2018, Nutrient sensing, growth and senescence, FEBS J., 285, 1948, 10.1111/febs.14400 · DOI
- Cassidy, 2022, Autophagy at the intersection of aging, senescence, and cancer, Mol. Oncol., 16, 3259, 10.1002/1878-0261.13269 · DOI
- Luo, 2009, Principles of cancer therapy: oncogene and non-oncogene addiction, Cell, 136, 823, 10.1016/j.cell.2009.02.024 · DOI · Paper page
- Pohl, 2019, Cellular quality control by the ubiquitin-proteasome system and autophagy, Science, 366, 818, 10.1126/science.aax3769 · DOI · Paper page
- Aliabadi, 2021, Ubiquitin-proteasome system and the role of its inhibitors in cancer therapy, Open Biol., 11, 10.1098/rsob.200390 · DOI
- Iriki, 2023, Senescent cells form nuclear foci that contain the 26S proteasome, Cell Rep., 42, 10.1016/j.celrep.2023.112880 · DOI
- Kwon, 2017, Autophagy is pro-senescence when seen in close-up, but anti-senescence in long-shot, Mol. Cells, 40, 607, 10.14348/molcells.2017.0151 · DOI
- Kim, 2021, All cells are created equal in the sight of autophagy: selective autophagy maintains homeostasis in senescent cells, Autophagy, 17, 3260, 10.1080/15548627.2021.1953848 · DOI
- Xu, 2020, SIRT1 is downregulated by autophagy in senescence and ageing, Nat. Cell Biol., 22, 1170, 10.1038/s41556-020-00579-5 · DOI
- Hao, 2022, ADAR1 downregulation by autophagy drives senescence independently of RNA editing by enhancing p16INK4a levels, Nat. Cell Biol., 24, 1202, 10.1038/s41556-022-00959-z · DOI
- Lopez, 2023, Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence, Cell Rep., 42, 10.1016/j.celrep.2023.113381 · DOI
- Ryu, 2023, The Bcl-2/Bcl-xL inhibitor ABT-263 attenuates retinal degeneration by selectively inducing apoptosis in senescent retinal pigment epithelial cells, Mol Cells, 46, 420, 10.14348/molcells.2023.2188 · DOI
- Junaid, 2022, Transcriptional heterogeneity of cellular senescence in cancer, Mol Cells, 45, 610, 10.14348/molcells.2022.0036 · 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
- Chan, 2019, Short-term gain, long-term pain: the senescence life cycle and cancer, Genes Dev., 33, 127, 10.1101/gad.320937.118 · DOI · Paper page
- Lee, 2019, The dynamic nature of senescence in cancer, Nat. Cell Biol., 21, 94, 10.1038/s41556-018-0249-2 · DOI · Paper page
- de Paula, 2023, Targeting senescence as a therapeutic opportunity for triple-negative breast cancer, Mol. Cancer Ther., 22, 583, 10.1158/1535-7163.MCT-22-0643 · DOI
Cited by
Sorted by citations
Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming
Zhang, W., Song, S., Zhang, Y., Pan, Y., Hu, D., & Wang, Y. (2026) · npj Aging · doi:10.1038/s41514-026-00355-z · Cited by 6
Metadata
- Authors
- Kim, Y., Jang, Y., Kim, M.-S., & Kang, C.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2024-08
- Volume
- 35
- Issue
- 8
- Pages
- 732-744
- ISSN
- 1043-2760
- Cited by
- 36
- References
- 34
- Language
- en
- Licence
- Funders
- National Research Foundation of Korea (NRF-2020R1A5A1018081, RS-2023-00246366, RS-2023-00275353, NRF-2022R1A2C3011850)
- Samsung Science & Technology Foundation (SSTF-BA2201 -09)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review