Сенотерапевтики: различия между версиями

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* Pollock, K., Dahlenburg, H., Nelson, H., Fink, K. D., Cary, W., Hendrix, K., ... & Nacey, C. (2016). Human Mesenchymal Stem Cells Genetically Engineered to Overexpress Brain-derived Neurotrophic Factor Improve Outcomes in Huntington's disease Mouse Models. Molecular therapy: the journal of the American Society of Gene Therapy. {{DOI|10.1038/mt.2016.12}}
* Pollock, K., Dahlenburg, H., Nelson, H., Fink, K. D., Cary, W., Hendrix, K., ... & Nacey, C. (2016). Human Mesenchymal Stem Cells Genetically Engineered to Overexpress Brain-derived Neurotrophic Factor Improve Outcomes in Huntington's disease Mouse Models. Molecular therapy: the journal of the American Society of Gene Therapy. {{DOI|10.1038/mt.2016.12}}
* Soto-Gamez A, Demaria M (2017). Therapeutic interventions for aging: the case of cellular senescence. Drug Discovery Today. {{doi|10.1016/j.drudis.2017.01.004}}
* Soto-Gamez A, Demaria M (2017). Therapeutic interventions for aging: the case of cellular senescence. Drug Discovery Today. {{doi|10.1016/j.drudis.2017.01.004}}
* Menendez, J. A., & Alarcón, T. (2017). [http://europepmc.org/articles/pmc5418360 Senescence-Inflammatory Regulation of Reparative Cellular Reprogramming in Aging and Cancer]. Front Cell Dev Biol.; 5: 49. {{doi|10.3389/fcell.2017.00049}} {{PMC|5418360}}
[[Категория:Геронтология]]
[[Категория:Геронтология]]
[[Категория:Лекарственные средства|*]]
[[Категория:Лекарственные средства|*]]

Версия от 08:08, 1 сентября 2017

Сенотерапевтики (англ. Senotherapeutics) это лечебные средства / стратегии, предназначенные для лечения клеточного старения[1][2].

К сенотерапевтикам относятся:

1. геропротекторы - средства для профилактики старения путём ослабления таких триггеров старения как: повреждение ДНК[3][4] , окислительный стресс[5], протеотоксический стресс[6], повреждение теломер[7];

2. агенты, препятствующие секреции SASP (senescence‐associated secretory phenotype)[8][9], включая:

3. средства / стратегии предназначенные для уничтожения постаревших клеток: сенолитики - малые молекулы, которые специфически индуцируют гибель стареющих клеток[16][17], антитела и опосредованная ими доставка лекарств, агенты, которые могут препятствовать ослаблению иммунной системы при старении[18], клетки иммунной системы (NK-клетки, В-клетки[19], Т-клетки).

4. средства / стратегии генной терапии предназначенные для редактирования генов организма с целью повышения его устойчивости к старению, старческим заболеваниям[20] и продления его жизни[21][21][22][23][24][25][26][27][28][29][30][31].

Примечания

  1. ↑ Childs et al. (2015). Cellular senescence in aging and age-related disease: from mechanisms to therapy Nature Medicine {{doi:10.1038/nm.4000}}
  2. ↑ Jafari Mahtab (2015). Healthspan Pharmacology. Rejuvenation Research., 18(6): 573-580. doi:10.1089/rej.2015.1774.
  3. ↑ Misra, J., Mohanty, S. T., Madan, S., Fernandes, J. A., Hal Ebetino, F., Russell, R. G. G. and Bellantuono, I. (2015), Zoledronate Attenuates Accumulation of DNA Damage in Mesenchymal Stem Cells and Protects Their Function. STEM CELLS. doi:10.1002/stem.2255
  4. ↑ Wahlestedt, M., Pronk, C. J., & Bryder, D. (2015). Concise Review: Hematopoietic Stem Cell Aging and the Prospects for Rejuvenation. Stem cells translational medicine, 4(2), 186-194.
  5. ↑ Eisenberg, T., Knauer, H., Schauer, A., Büttner, S., Ruckenstuhl, C., Carmona-Gutierrez, D., ... & Fussi, H. (2009). Induction of autophagy by spermidine promotes longevity. Nature cell biology, 11(11), 1305-1314. doi:10.1038/ncb1975
  6. ↑ Pride, H., Yu, Z., Sunchu, B., Mochnick, J., Coles, A., Zhang, Y., ... & Pérez, V. I. (2015). Long-lived species have improved proteostasis compared to phylogenetically-related shorter-lived species. Biochemical and biophysical research communications, 457(4), 669-675. doi:10.1016/j.bbrc.2015.01.046
  7. ↑ Blackburn, E. H., Epel, E. S., & Lin, J. (2015). Human telomere biology: A contributory and interactive factor in aging, disease risks, and protection. Science, 350(6265), 1193-1198. doi:10.1126/science.aab3389
  8. ↑ Hae-Ok, B., & Gyesoon, Y. (2015). From cell senescence to age-related diseases: differential mechanisms of action of senescence-associated secretory phenotypes. BMB reports, 48(10), 549-558. PMID 26129674
  9. ↑ Young, A. R., & Narita, M. (2009). SASP reflects senescence. EMBO reports, 10(3), 228-230. doi:10.1038/embor.2009.22
  10. ↑ Laberge, R. M., Zhou, L., Sarantos, M. R., Rodier, F., Freund, A., de Keizer, P. L., ... & Desprez, P. Y. (2012). Glucocorticoids suppress selected components of the senescence‐associated secretory phenotype. Aging cell, 11(4), 569-578. doi:10.1111/j.1474-9726.2012.00818.x
  11. ↑ Liu, S., Uppal, H., Demaria, M., Desprez, P. Y., Campisi, J., & Kapahi, P. (2015). Simvastatin suppresses breast cancer cell proliferation induced by senescent cells. Scientific reports, 5, 17895. doi:10.1038/srep17895
  12. ↑ Xu, M., Tchkonia, T., Ding, H., Ogrodnik, M., Lubbers, E. R., Pirtskhalava, T., ... & Giorgadze, N. (2015). JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age. Proceedings of the National Academy of Sciences, 112(46), E6301-E6310, doi: 10.1073/pnas.1515386112
  13. ↑ Xu, M., Palmer, A. K., Ding, H., Weivoda, M. M., Pirtskhalava, T., White, T. A., ... & Jensen, M. D. (2015). Targeting senescent cells enhances adipogenesis and metabolic function in old age. eLife, e12997. DOI: http://dx.doi.org/10.7554/eLife.12997
  14. ↑ Sébastien Cardinal et al., & Normand Voyer (2017). Synthesis and anti-inflammatory activity of isoquebecol. Bioorganic & Medicinal Chemistry
  15. ↑ Correia-Melo C, Marques FD, Anderson R, et al., & Passos JF (2016). Mitochondria are required for pro-ageing features of the senescent phenotype. The EMBO Journal, PMID 26848154, doi:10.15252/embj.201592862
  16. ↑ Chang J., Wang Y.,Shao L. et al., & Zhou D. (2015). Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice. Nature Medicine doi:10.1038/nm.4010
  17. ↑ Zhu, Yi; Tchkonia, Tamara; Pirtskhalava, Tamar; et al., (2015). The Achilles’ Heel of Senescent Cells: From Transcriptome to Senolytic Drugs. Aging Cell. doi:10.1111/acel.12344
  18. ↑ Stahl, E. C., & Brown, B. N. (2015). Cell Therapy Strategies to Combat Immunosenescence. Organogenesis, (just-accepted), doi:10.1080/15476278.2015.1120046
  19. ↑ Henry, C. J., Casás-Selves, M., Kim, J., Zaberezhnyy, V., Aghili, L., Daniel, A. E., ... & Klawitter, J. (2015). Aging-associated inflammation promotes selection for adaptive oncogenic events in B cell progenitors. The Journal of clinical investigation, 125(12),
  20. ↑ Fortney K, Dobriban E, Garagnani P, Pirazzini C, Monti D, Mari D, et al. (2015) Genome-Wide Scan Informed by Age-Related Disease Identifies Loci for Exceptional Human Longevity. PLoS Genet 11(12): e1005728. doi:10.1371/journal.pgen.1005728
  21. ↑ 1 2 Andrews, W. H., Brown, L. K., Mohammadpour, H., & Briggs, L. A. (2015). Enhancing Health in Mammals Using Telomerase Reverse Transcriptase Gene Therapy. U.S. Patent No. 20,150,322,416. Washington, DC: U.S. Patent and Trademark Office.
  22. ↑ de Jesus, B. B., Vera, E., Schneeberger, K., Tejera, A. M., Ayuso, E., Bosch, F., & Blasco, M. A. (2012). Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO molecular medicine, 4(8), 691-704. doi:10.1002/emmm.201200245
  23. ↑ Xiong, S., Patrushev, N., Forouzandeh, F., Hilenski, L., & Alexander, R. W. (2015). PGC-1α modulates telomere function and DNA damage in protecting against aging-related chronic diseases. Cell reports, 12(9), 1391-1399. doi:10.1016/j.celrep.2015.07.047
  24. ↑ Mendelsohn Andrew R. and Larrick James W. (2015). Telomerase Reverse Transcriptase and Peroxisome Proliferator-Activated Receptor γ Co-Activator-1α Cooperate to Protect Cells from DNA Damage and Mitochondrial Dysfunction in Vascular Senescence. Rejuvenation Research., 18(5): 479-483. doi:10.1089/rej.2015.1780.
  25. ↑ Hofmann, J. W., Zhao, X., De Cecco, M., Peterson, A. L., Pagliaroli, L., Manivannan, J., ... & Li, X. (2015). Reduced expression of MYC increases longevity and enhances healthspan. Cell, 160(3), 477-488. doi:10.1016/j.cell.2014.12.016
  26. ↑ Wu, J. J., Liu, J., Chen, E. B., Wang, J. J., Cao, L., Narayan, N., ... & Finkel, T. (2013). Increased mammalian lifespan and a segmental and tissue-specific slowing of aging after genetic reduction of mTOR expression. Cell reports, 4(5), 913-920 doi:10.1016/j.celrep.2013.07.030
  27. ↑ Kirkland, J. L., Tchkonia, T., Van Deursen, J., & Baker, D. J. (2015). TRANSGENIC ANIMALS CAPABLE OF BEING INDUCED TO DELETE SENESCENT CELLS. U.S. Patent No. 20,150,296,755. Washington, DC: U.S. Patent and Trademark Office
  28. ↑ Yun-Hee Youm, Tamas L. Horvath, David J. Mangelsdorf, Steven A. Kliewer, and Vishwa Deep Dixit (2016).Prolongevity hormone FGF21 protects against immune senescence by delaying age-related thymic involution. PNAS doi:10.1073/pnas.1514511113
  29. ↑ Sun, H., Gao, Y., Lu, K., Zhao, G., Li, X., Li, Z., & Chang, H. (2015). Overexpression of Klotho suppresses liver cancer progression and induces cell apoptosis by negatively regulating wnt/β-catenin signaling pathway. World journal of surgical oncology, 13(1), 307 doi:10.1186/s12957-015-0717-0
  30. ↑ Kurosu, H., Yamamoto, M., Clark, J. D., Pastor, J. V., Nandi, A., Gurnani, P., ... & Shimomura, I. (2005). Suppression of aging in mice by the hormone Klotho. Science, 309(5742), 1829-1833 doi:10.1126/science.1112766
  31. ↑ Yan, L., Vatner, D. E., O'Connor, J. P., Ivessa, A., Ge, H., Chen, W., ... & Vatner, S. F. (2007). Type 5 adenylyl cyclase disruption increases longevity and protects against stress. Cell, 130(2), 247-258 doi:10.1016/j.cell.2007.05.038

Литература

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  • Pollock, K., Dahlenburg, H., Nelson, H., Fink, K. D., Cary, W., Hendrix, K., ... & Nacey, C. (2016). Human Mesenchymal Stem Cells Genetically Engineered to Overexpress Brain-derived Neurotrophic Factor Improve Outcomes in Huntington's disease Mouse Models. Molecular therapy: the journal of the American Society of Gene Therapy. doi:10.1038/mt.2016.12
  • Soto-Gamez A, Demaria M (2017). Therapeutic interventions for aging: the case of cellular senescence. Drug Discovery Today. doi:10.1016/j.drudis.2017.01.004
  • Menendez, J. A., & Alarcón, T. (2017). Senescence-Inflammatory Regulation of Reparative Cellular Reprogramming in Aging and Cancer. Front Cell Dev Biol.; 5: 49. doi:10.3389/fcell.2017.00049 PMC 5418360
Источник — https://ru.wikipedia.org/w/index.php?title=Сенотерапевтики&oldid=87374422