Возрастные изменения и потеря устойчивости почечной ткани к повреждениям: роль снижения количества прогениторных клеток почки при старении
https://doi.org/10.37586/2949-4745-3-2023-127-133
Аннотация
В процессе старения многие органы претерпевают негативные изменения, ухудшающие их функционирование и способность к регенерации. В частности, почки с возрастом становятся более уязвимыми к острому повреждению, и повышается вероятность его перехода в хроническую болезнь почек. Во многом это может быть обусловлено снижением количества резидентных прогениторных клеток почки. В данном обзоре рассмотрены возрастные изменения, происходящие в почках на гистологическом и молекулярном уровнях, в том числе связанные с клеточным циклом, функционированием митохондрий, окислительным стрессом и хроническим воспалением. В данном обзоре описаны имеющиеся исследования резидентных стволовых клеток почек, их ниши, морфология, возможные маркеры, а также динамика их количества в процессе старения организма. На основе молекулярных и клеточных механизмов рассматриваются причины возрастного снижения регенеративного потенциала почек.
Ключевые слова
При поддержке: Работа поддержана Российским научным фондом (грант 21-75-30009).
Об авторах
М. И. Буян
МГУ им. М.В. Ломоносова
Россия
Россия
Буян Марина Игоревна, младший научный сотрудник, Факультет биоинженерии и биоинформатики
Москва
Н. В. Андрианова
НИИ физико-химической биологии имени А.Н. Белозерского, МГУ им. М.В. Ломоносова
Россия
Россия
Андрианова Надежда Владимировна, канд. биол. наук, научный сотрудник лаборатории структуры и функций митохондрий
Москва
Е. Ю. Плотников
НИИ физико-химической биологии имени А.Н. Белозерского, МГУ им. М.В. Ломоносова
Россия
Россия
Плотников Егор Юрьевич, д-р биол. наук, профессор РАН, заведующий лабораторией структуры и функций митохондрий
Телефон: +7(495)939-59-44
Москва
Список литературы
1. Ferenbach D.A., Bonventre J.V. Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD // Nat. Rev. Nephrol. 2015. Vol. 11, № 5. P. 264–276.
2. Gros J. et al. A common somitic origin for embryonic muscle progenitors and satellite cells // Nature. 2005. Vol. 435, № 7044. P. 954–958.
3. Apple D.M., Solano-Fonseca R., Kokovay E. Neurogenesis in the aging brain // Biochem. Pharmacol. 2017. Vol. 141. P. 77–85.
4. Jasper H. Intestinal Stem Cell Aging: Origins and Interventions // Annu. Rev. Physiol. 2020. Vol. 82. P. 203–226.
5. Nyengaard J.R., Bendtsen T.F. Glomerular number and size in relation to age, kidney weight, and body surface in normal man // Anat. Rec. 1992. Vol. 232, № 2. P. 194–201.
6. Rule A.D. et al. The association between age and nephrosclerosis on renal biopsy among healthy adults // Ann. Intern. Med. 2010. Vol. 152, № 9. P. 561–567.
7. Rule A.D., Cornell L.D., Poggio E.D. Senile nephrosclerosis- -does it explain the decline in glomerular filtration rate with aging? // Nephron Physiol. 2011. Vol. 119 Suppl 1. P. 6–11.
8. Wang X., Bonventre J.V., Parrish A.R. The aging kidney: increased susceptibility to nephrotoxicity // Int. J. Mol. Sci. 2014. Vol. 15, № 9. P. 15358–15376.
9. Yang H., Fogo A.B. Cell senescence in the aging kidney // J. Am. Soc. Nephrol. 2010. Vol. 21, № 9. P. 1436–1439.
10. Braun H. et al. Cellular senescence limits regenerative capacity and allograft survival // J. Am. Soc. Nephrol. 2012. Vol. 23, № 9. P. 1467–1473.
11. Yang L. et al. Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury // Nat. Med. 2010. Vol. 16, № 5. P. 535–543, 1p following 143.
12. van Deursen J.M. The role of senescent cells in ageing // Nature. 2014. Vol. 509, № 7501. P. 439–446.
13. Kang D.H. et al. Impaired angiogenesis in the aging kidney: vascular endothelial growth factor and thrombospondin-1 in renal disease // Am. J. Kidney Dis. 2001. Vol. 37, № 3. P. 601–611.
14. Ruiz-Torres M.P. et al. Age-related increase in expression of TGF-beta1 in the rat kidney: relationship to morphologic changes // J. Am. Soc. Nephrol. 1998. Vol. 9, № 5. P. 782–791.
15. Thakar C.V. et al. Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia // J. Clin. Invest. 2005. Vol. 115, № 12. P. 3451–3459.
16. Liguori I. et al. Oxidative stress, aging, and diseases // Clin. Interv. Aging. 2018. Vol. 13. P. 757–772.
17. Locatelli F. et al. Oxidative stress in end-stage renal disease: an emerging threat to patient outcome // Nephrol. Dial. Transplant. 2003. Vol. 18, № 7. P. 1272–1280.
18. Birben E. et al. Oxidative stress and antioxidant defense // World Allergy Organ. J. 2012. Vol. 5, № 1. P. 9–19.
19. Himmelfarb J. Relevance of oxidative pathways in the pathophysiology of chronic kidney disease // Cardiol. Clin. 2005. Vol. 23, № 3. P. 319–330.
20. Nistala R., Whaley-Connell A., Sowers J.R. Redox control of renal function and hypertension // Antioxid. Redox Signal. 2008. Vol. 10, № 12. P. 2047–2089.
21. Tbahriti H.F. et al. Effect of different stages of chronic kidney disease and renal replacement therapies on oxidant-antioxidant balance in uremic patients // Biochem. Res. Int. 2013. Vol. 2013. P. 358985.
22. Jankauskas S.S. et al. The age-associated loss of ischemic preconditioning in the kidney is accompanied by mitochondrial dysfunction, increased protein acetylation and decreased autophagy // Sci. Rep. 2017. Vol. 7. P. 44430.
23. Choksi K.B. et al. Age-related increases in oxidatively damaged proteins of mouse kidney mitochondrial electron transport chain complexes // Free Radic. Biol. Med. 2007. Vol. 43, № 10. P. 1423–1438.
24. Qiao X. et al. Mitochondrial pathway is responsible for aging-related increase of tubular cell apoptosis in renal ischemia/reperfusion injury // J. Gerontol. A Biol. Sci. Med. Sci. 2005. Vol. 60, № 7. P. 830–839.
25. Serviddio G. et al. Bioenergetics in aging: mitochondrial proton leak in aging rat liver, kidney and heart // Redox Rep. 2007. Vol. 12, № 1. P. 91–95.
26. Ferrucci L., Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty // Nat. Rev. Cardiol. 2018. Vol. 15, № 9. P. 505–522.
27. Shlipak M.G. et al. Elevations of inflammatory and procoagulant biomarkers in elderly persons with renal insufficiency // Circulation. 2003. Vol. 107, № 1. P. 87–92.
28. Kolios G., Moodley Y. Introduction to stem cells and regenerative medicine // Respiration. 2013. Vol. 85, № 1. P. 3–10.
29. Ferraro F., Celso C.L., Scadden D. Adult stem cels and their niches // Adv. Exp. Med. Biol. 2010. Vol. 695. P. 155–168.
30. Andrianova N.V. et al. Kidney Cells Regeneration: Dedifferentiation of Tubular Epithelium, Resident Stem Cells and Possible Niches for Renal Progenitors // Int. J. Mol. Sci. 2019. Vol. 20, № 24.
31. Oliver J.A. et al. The renal papilla is a niche for adult kidney stem cells // J. Clin. Invest. 2004. Vol. 114, № 6. P. 795–804.
32. Patschan D. et al. Normal distribution and medullary-to-cortical shift of Nestin-expressing cells in acute renal ischemia // Kidney Int. 2007. Vol. 71, № 8. P. 744–754.
33. Mohyeldin A., Garz?n-Muvdi T., Qui?ones-Hinojosa A. Oxygen in stem cell biology: a critical component of the stem cell niche // Cell Stem Cell. 2010. Vol. 7, № 2. P. 150–161.
34. Pannabecker T.L., Layton A.T. Targeted delivery of solutes and oxygen in the renal medulla: role of microvessel architecture // Am. J. Physiol. Renal Physiol. 2014. Vol. 307, № 6. P. F649–F655.
35. Huling J., Yoo J.J. Comparing adult renal stem cell identification, characterization and applications // J. Biomed. Sci. 2017. Vol. 24, № 1. P. 32.
36. Grange C. et al. Protective effect and localization by optical imaging of human renal CD133+ progenitor cells in an acute kidney injury model // Physiol Rep. 2014. Vol. 2, № 5. P. e12009.
37. Smeets B. et al. Proximal tubular cells contain a phenotypically distinct, scattered cell population involved in tubular regeneration // J. Pathol. 2013. Vol. 229, № 5. P. 645–659.
38. Gupta S. et al. Isolation and characterization of kidney-derived stem cells // J. Am. Soc. Nephrol. 2006. Vol. 17, № 11. P. 3028–3040.
39. Kitamura S., Sakurai H., Makino H. Single adult kidney stem/ progenitor cells reconstitute three-dimensional nephron structures in vitro // Stem Cells. 2015. Vol. 33, № 3. P. 774–784.
40. Abedin M.J. et al. Identification and characterization of Sall1- expressing cells present in the adult mouse kidney // Nephron Exp. Nephrol. 2011. Vol. 119, № 4. P. e75–e82.
41. Lazzeri E. et al. Endocycle-related tubular cell hypertrophy and progenitor proliferation recover renal function after acute kidney injury // Nat. Commun. 2018. Vol. 9, № 1. P. 1344.
42. Ward H.H. et al. Adult human CD133/1(+) kidney cells isolated from papilla integrate into developing kidney tubules // Biochim. Biophys. Acta. 2011. Vol. 1812, № 10. P. 1344–1357.
43. Folmes C.D.L. et al. Metabolic plasticity in stem cell homeostasis and differentiation // Cell Stem Cell. 2012. Vol. 11, № 5. P. 596–606.
44. Takubo K. et al. Regulation of glycolysis by Pdk functions as a metabolic checkpoint for cell cycle quiescence in hematopoietic stem cells // Cell Stem Cell. 2013. Vol. 12, № 1. P. 49–61.
45. Piccoli C. et al. Characterization of mitochondrial and extra-mitochondrial oxygen consuming reactions in human hematopoietic stem cells. Novel evidence of the occurrence of NAD(P)H oxidase activity // J. Biol. Chem. 2005. Vol. 280, № 28. P. 26467–26476.
46. Sahin E., Depinho R.A. Linking functional decline of telomeres, mitochondria and stem cells during ageing // Nature. 2010. Vol. 464, № 7288. P. 520–528.
47. Ahlqvist K.J. et al. Somatic progenitor cell vulnerability to mitochondrial DNA mutagenesis underlies progeroid phenotypes in Polg mutator mice // Cell Metab. 2012. Vol. 15, № 1. P. 100–109.
48. Morganti C. et al. Electron transport chain complex II sustains high mitochondrial membrane potential in hematopoietic stem and progenitor cells // Stem Cell Res. 2019. Vol. 40. P. 101573.
49. Sukumar M. et al. Mitochondrial Membrane Potential Identifies Cells with Enhanced Stemness for Cellular Therapy // Cell Metab. 2016. Vol. 23, № 1. P. 63–76.
50. Prigione A. et al. Mitochondrial-associated cell death mechanisms are reset to an embryonic-like state in aged donor-derived iPS cells harboring chromosomal aberrations // PLoS One. 2011. Vol. 6, № 11. P. e27352.
51. Ito K. et al. Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells // Nature. 2004. Vol. 431, № 7011. P. 997–1002.
52. Garcia-Prat L. et al. FoxO maintains a genuine muscle stem-cell quiescent state until geriatric age // Nat. Cell Biol. 2020. Vol. 22, № 11. P. 1307–1318.
53. Yin H., Price F., Rudnicki M.A. Satellite cells and the muscle stem cell niche // Physiol. Rev. 2013. Vol. 93, № 1. P. 23–67.
54. Garcia-Prat L., Mu?oz-C?noves P. Aging, metabolism and stem cells: Spotlight on muscle stem cells // Mol. Cell. Endocrinol. 2017. Vol. 445. P. 109–117.
55. Sousa-Victor P. et al. Geriatric muscle stem cells switch reversible quiescence into senescence // Nature. 2014. Vol. 506, № 7488. P. 316–321.
56. Hwang A.B., Brack A.S. Muscle Stem Cells and Aging // Curr. Top. Dev. Biol. 2018. Vol. 126. P. 299–322.
57. Yamakawa H. et al. Stem Cell Aging in Skeletal Muscle Regeneration and Disease // International Journal of Molecular Sciences. 2020. Vol. 21, № 5. P. 1830.
58. Katsimpardi L., Lledo P.-M. Regulation of neurogenesis in the adult and aging brain // Curr. Opin. Neurobiol. 2018. Vol. 53. P. 131–138.
59. Isaev N.K., Stelmashook E.V., Genrikhs E.E. Neurogenesis and brain aging // Rev. Neurosci. 2019. Vol. 30, № 6. P. 573–580.
60. Lewis-McDougall F.C. et al. Aged-senescent cells contribute to impaired heart regeneration // Aging Cell. 2019. Vol. 18, № 3. P. e12931.
61. Cianflone E. et al. Targeting Cardiac Stem Cell Senescence to Treat Cardiac Aging and Disease // Cells. 2020. Vol. 9, № 6.
62. Kozar S. et al. Continuous clonal labeling reveals small numbers of functional stem cells in intestinal crypts and adenomas // Cell Stem Cell. 2013. Vol. 13, № 5. P. 626–633.
63. Nalapareddy K. et al. Canonical Wnt Signaling Ameliorates Aging of Intestinal Stem Cells // Cell Rep. 2017. Vol. 18, № 11. P. 2608–2621.
64. Schmitt R., Cantley L.G. The impact of aging on kidney repair // Am. J. Physiol. Renal Physiol. 2008. Vol. 294, № 6. P. F1265–F1272.
65. Miya M. et al. Age-related decline in label-retaining tubular cells: implication for reduced regenerative capacity after injury in the aging kidney // Am. J. Physiol. Renal Physiol. 2012. Vol. 302, № 6. P. F694–F702.
66. Buyan M.I. et al. Age-Associated Loss in Renal Nestin-Positive Progenitor Cells // Int. J. Mol. Sci. 2022. Vol. 23, № 19.
67. Wiese C. et al. Nestin expression--a property of multi-lineage progenitor cells? // Cell. Mol. Life Sci. 2004. Vol. 61, № 19-20. P. 2510–2522.
68. Lopez-Otin C. et al. The hallmarks of aging // Cell. 2013. Vol. 153, № 6. P. 1194–1217.
69. Jankauskas S.S. et al. Aged kidney: can we protect it? Autophagy, mitochondria and mechanisms of ischemic preconditioning // Cell Cycle. 2018. Vol. 17, № 11. P. 1291–1309.
Рецензия
Для цитирования:
Буян М.И., Андрианова Н.В., Плотников Е.Ю. Возрастные изменения и потеря устойчивости почечной ткани к повреждениям: роль снижения количества прогениторных клеток почки при старении. Проблемы геронауки. 2023;(3):127-133. https://doi.org/10.37586/2949-4745-3-2023-127-133
For citation:
Buyan M.I., Andrianova N.V., Plotnikov E.Y. Age-Related Changes in Kidney and Loss of Resistance to Damage: The Role of the Decrease in the Number of Kidney Progenitor Cells during Aging. Problems of Geroscience. 2023;(3):127-133. (In Russ.) https://doi.org/10.37586/2949-4745-3-2023-127-133
Просмотров:
247
Послать статью по эл. почте .jpg)
