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Implication of cellular senescence in the progression of chronic kidney disease and the treatment potencies

Wang, Yao, Wang, Ying, Yang, Ming, Ma, Xingjie·2021·Biomedicine & Pharmacotherapy
DOI 10.1016/j.biopha.2020.111191
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  1. Stenvinkel, 2013, Chronic kidney disease: a clinical model of premature aging, Am. J. Kidney Dis., 62, 339, 10.1053/j.ajkd.2012.11.051 · DOI
  2. 2011, Kidney disease: improving global outcomes CKDMBDUWG: KDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD), Kidney Int. Suppl., 2017, 1
  3. Dai, 2019, Early vascular ageing and cellular senescence in chronic kidney disease, Comput. Struct. Biotechnol. J., 17, 721, 10.1016/j.csbj.2019.06.015 · DOI
  4. O’Sullivan, 2017, Renal aging: causes and consequences, J. Am. Soc. Nephrol., 28, 407, 10.1681/ASN.2015121308 · DOI · Paper page
  5. Campisi, 2007, Cellular senescence: when bad things happen to good cells, Nat. Rev. Mol. Cell Biol., 8, 729, 10.1038/nrm2233 · DOI · Paper page
  6. el-Deiry, 1993, WAF1, a potential mediator of p53 tumor suppression, Cell, 75, 817, 10.1016/0092-8674(93)90500-P · DOI · Paper page
  7. Canaud, 2015, Cell cycle arrest and the evolution of chronic kidney disease from acute kidney injury, Nephrol. Dial. Transplant., 30, 575, 10.1093/ndt/gfu230 · DOI
  8. Hubackova, 2012, IL1- and TGFbeta-Nox4 signaling, oxidative stress and DNA damage response are shared features of replicative, oncogene-induced, and drug-induced paracrine’ bystander senescence’, Aging (Albany NY), 4, 932, 10.18632/aging.100520 · DOI · Paper page
  9. Iwasa, 2003, Mitogen-activated protein kinase p38 defines the common senescence-signalling pathway, Genes Cells, 8, 131, 10.1046/j.1365-2443.2003.00620.x · DOI
  10. Chien, 2011, Control of the senescence-associated secretory phenotype by NF-kappaB promotes senescence and enhances chemosensitivity, Genes Dev., 25, 2125, 10.1101/gad.17276711 · DOI · Paper page
  11. Yosef, 2017, p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling, EMBO J., 36, 2280, 10.15252/embj.201695553 · DOI · Paper page
  12. Fuhrmann-Stroissnigg, 2017, Identification of HSP90 inhibitors as a novel class of senolytics, Nat. Commun., 8, 422, 10.1038/s41467-017-00314-z · DOI · Paper page
  13. Megyesi, 1999, The lack of a functional p21(WAF1/CIP1) gene ameliorates progression to chronic renal failure, Proc. Natl. Acad. Sci. U. S. A., 96, 10830, 10.1073/pnas.96.19.10830 · DOI
  14. Verzola, 2008, Accelerated senescence in the kidneys of patients with type 2 diabetic nephropathy, Am. J. Physiol. Renal Physiol., 295, F1563, 10.1152/ajprenal.90302.2008 · DOI · Paper page
  15. Lee, 2012, INK4a deletion results in improved kidney regeneration and decreased capillary rarefaction after ischemia-reperfusion injury, Am. J. Physiol. Renal Physiol., 302, F183, 10.1152/ajprenal.00407.2011 · DOI
  16. Braun, 2012, Cellular senescence limits regenerative capacity and allograft survival, J. Am. Soc. Nephrol., 23, 1467, 10.1681/ASN.2011100967 · DOI
  17. Schmitz, 2016, Cyclin-dependent kinases as coregulators of inflammatory gene expression, Trends Pharmacol. Sci., 37, 101, 10.1016/j.tips.2015.10.004 · DOI
  18. Murakami, 2012, p16(INK4a) exerts an anti-inflammatory effect through accelerated IRAK1 degradation in macrophages, J. Immunol., 189, 5066, 10.4049/jimmunol.1103156 · DOI
  19. Sorensen-Zender, 2014, Renal tubular Notch signaling triggers a prosenescent state after acute kidney injury, Am. J. Physiol. Renal Physiol., 306, F907, 10.1152/ajprenal.00030.2014 · DOI
  20. Lim, 2013, Outcomes of kidney transplantation from older living donors, Transplantation, 95, 106, 10.1097/TP.0b013e318277b2be · DOI
  21. Prattichizzo, 2018, Short-term sustained hyperglycaemia fosters an archetypal senescence-associated secretory phenotype in endothelial cells and macrophages, Redox Biol., 15, 170, 10.1016/j.redox.2017.12.001 · DOI · Paper page
  22. Mayer, 2011, Capillary rarefaction, hypoxia, VEGF and angiogenesis in chronic renal disease, Nephrol. Dial. Transplant., 26, 1132, 10.1093/ndt/gfq832 · DOI
  23. Sutariya, 2016, TGF-beta: the connecting link between nephropathy and fibrosis, Immunopharmacol. Immunotoxicol., 38, 39, 10.3109/08923973.2015.1127382 · DOI
  24. Reiss, 2018, CKD, arterial calcification, atherosclerosis and bone health: inter-relationships and controversies, Atherosclerosis, 278, 49, 10.1016/j.atherosclerosis.2018.08.046 · DOI
  25. Kendrick, 2011, The role of phosphorus in the development and progression of vascular calcification, Am. J. Kidney Dis., 58, 826, 10.1053/j.ajkd.2011.07.020 · DOI
  26. McClelland, 2016, Accelerated ageing and renal dysfunction links lower socioeconomic status and dietary phosphate intake, Aging (Albany NY), 8, 1135, 10.18632/aging.100948 · DOI
  27. Miao, 2019, Wnt/β-catenin/RAS signaling mediates age-related renal fibrosis and is associated with mitochondrial dysfunction, Aging Cell, 18, e13004, 10.1111/acel.13004 · DOI
  28. Benigni, 2009, Disruption of the Ang II type 1 receptor promotes longevity in mice, J. Clin. Invest., 119, 524, 10.1172/JCI36703 · DOI
  29. Jang, 2018, Effects of resveratrol on the renin-angiotensin system in the aging kidney, Nutrients, 10, 10.3390/nu10111741 · DOI · Paper page
  30. Sukhanov, 2011, Angiotensin II, oxidative stress and skeletal muscle wasting, Am. J. Med. Sci., 342, 143, 10.1097/MAJ.0b013e318222e620 · DOI
  31. Marzetti, 2013, Late-life enalapril administration induces nitric oxide-dependent and independent metabolic adaptations in the rat skeletal muscle, Age (Dordr), 35, 1061, 10.1007/s11357-012-9428-4 · DOI
  32. Tamaki, 2014, Chronic kidney disease reduces muscle mitochondria and exercise endurance and its exacerbation by dietary protein through inactivation of pyruvate dehydrogenase, Kidney Int., 85, 1330, 10.1038/ki.2013.473 · DOI
  33. Schilder, 2009, NADPH oxidases 1 and 4 mediate cellular senescence induced by resveratrol in human endothelial cells, Free Radic. Biol. Med., 46, 1598, 10.1016/j.freeradbiomed.2009.03.013 · DOI
  34. Zhu, 2015, NADPH oxidase NOX1 is involved in activation of protein kinase C and premature senescence in early stage diabetic kidney, Free Radic. Biol. Med., 83, 21, 10.1016/j.freeradbiomed.2015.02.009 · DOI
  35. Palm, 2008, How shelterin protects mammalian telomeres, Annu. Rev. Genet., 42, 301, 10.1146/annurev.genet.41.110306.130350 · DOI · Paper page
  36. Wills, 2011, Telomeres and telomerase in renal health, J. Am. Soc. Nephrol., 22, 39, 10.1681/ASN.2010060662 · DOI
  37. Lata, 2018, Whole-exome sequencing in adults with chronic kidney disease: a pilot study, Ann. Intern. Med., 168, 100, 10.7326/M17-1319 · DOI
  38. Hirashio, 2014, Telomeric g-tail length and hospitalization for cardiovascular events in hemodialysis patients, Clin. J. Am. Soc. Nephrol., 9, 2117, 10.2215/CJN.10010913 · DOI
  39. Ameh, 2017, Association between telomere length, chronic kidney disease, and renal traits: a systematic review, Omics, 21, 143, 10.1089/omi.2016.0180 · DOI
  40. Carrero, 2008, Telomere attrition is associated with inflammation, low fetuin-A levels and high mortality in prevalent haemodialysis patients, J. Intern. Med., 263, 302, 10.1111/j.1365-2796.2007.01890.x · DOI
  41. Gurung, 2018, Short leukocyte telomere length predicts albuminuria progression in individuals with type 2 diabetes, Kidney Int. Rep., 3, 592, 10.1016/j.ekir.2017.12.005 · DOI
  42. Kidir, 2017, Telomerase activity in patients with stage 2-5D chronic kidney disease, Nefrologia, 37, 592, 10.1016/j.nefro.2017.03.025 · DOI
  43. Cokan Vujkovac, 2019, Aging in fabry disease: role of telomere length, telomerase activity, and kidney disease, Nephron, 1
  44. Xiong, 2015, PGC-1alpha modulates telomere function and DNA damage in protecting against aging-related chronic diseases, Cell Rep., 12, 1391, 10.1016/j.celrep.2015.07.047 · DOI
  45. Rasbach, 2007, PGC-1alpha over-expression promotes recovery from mitochondrial dysfunction and cell injury, Biochem. Biophys. Res. Commun., 355, 734, 10.1016/j.bbrc.2007.02.023 · DOI
  46. Lee, 2019, PGC-1alpha, a potential therapeutic target against kidney aging, Aging Cell, 18, e12994, 10.1111/acel.12994 · DOI
  47. Chung, 2018, Impairment of PPARalpha and the fatty acid oxidation pathway aggravates renal fibrosis during aging, J. Am. Soc. Nephrol., 29, 1223, 10.1681/ASN.2017070802 · DOI
  48. Cheng, 2015, Telomerase deficiency delays renal recovery in mice after ischemia-reperfusion injury by impairing autophagy, Kidney Int., 88, 85, 10.1038/ki.2015.69 · DOI · Paper page
  49. Harris, 2016, Telomerase, autophagy and acute kidney injury, Nephron, 134, 145, 10.1159/000446665 · DOI
  50. Shi, 2016, αKlotho mitigates progression of AKI to CKD through activation of autophagy, J. Am. Soc. Nephrol. JASN, 27, 2331, 10.1681/ASN.2015060613 · DOI
  51. Zhang, 2019, C/EBPα deficiency in podocytes aggravates podocyte senescence and kidney injury in aging mice, Cell Death Dis., 10, 684, 10.1038/s41419-019-1933-2 · DOI · Paper page
  52. Lenoir, 2016, Autophagy in kidney disease and aging: lessons from rodent models, Kidney Int., 90, 950, 10.1016/j.kint.2016.04.014 · DOI
  53. Nakamura, 2019, Suppression of autophagic activity by Rubicon is a signature of aging, Nat. Commun., 10, 847, 10.1038/s41467-019-08729-6 · DOI · Paper page
  54. Erben, 2017, FGF23-Klotho signaling axis in the kidney, Bone, 100, 62, 10.1016/j.bone.2016.09.010 · DOI
  55. Keles, 2015, Low serum level of klotho is an early predictor of atherosclerosis, Tohoku J. Exp. Med., 237, 17, 10.1620/tjem.237.17 · DOI
  56. Yu, 2018, Circulating alpha-klotho levels in hemodialysis patients and their relationship to atherosclerosis, Kidney Blood Press. Res., 43, 1174, 10.1159/000492245 · DOI
  57. Kuro-o, 1997, Mutation of the mouse klotho gene leads to a syndrome resembling ageing, Nature, 390, 45, 10.1038/36285 · DOI · Paper page
  58. Arking, 2002, Association of human aging with a functional variant of klotho, Proc. Natl. Acad. Sci. U. S. A., 99, 856, 10.1073/pnas.022484299 · DOI
  59. Neyra, 2017, Potential application of klotho in human chronic kidney disease, Bone, 100, 41, 10.1016/j.bone.2017.01.017 · DOI
  60. Kimura, 2018, The impact of preserved Klotho gene expression on antioxidative stress activity in healthy kidney, Am. J. Physiol. Renal Physiol., 315, F345, 10.1152/ajprenal.00486.2017 · DOI
  61. Guarente, 2011, Franklin H. Epstein lecture: sirtuins, aging, and medicine, N. Engl. J. Med., 364, 2235, 10.1056/NEJMra1100831 · DOI · Paper page
  62. Li, 2010, Resveratrol inhibits renal fibrosis in the obstructed kidney: potential role in deacetylation of Smad3, Am. J. Pathol., 177, 1065, 10.2353/ajpath.2010.090923 · DOI
  63. Kida, 2016, Endothelial sirtuin 1 inactivation enhances capillary rarefaction and fibrosis following kidney injury through Notch activation, Biochem. Biophys. Res. Commun., 478, 1074, 10.1016/j.bbrc.2016.08.066 · DOI
  64. Schafer, 2018, Targeting senescent cells in fibrosis: pathology, paradox, and practical considerations, Curr. Rheumatol. Rep., 20, 3, 10.1007/s11926-018-0712-x · DOI
  65. Baar, 2017, Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging, Cell, 169, 132, 10.1016/j.cell.2017.02.031 · DOI · Paper page
  66. Rubinsztein, 2011, Autophagy and aging, Cell, 146, 682, 10.1016/j.cell.2011.07.030 · DOI · Paper page
  67. Ning, 2013, Short-term calorie restriction protects against renal senescence of aged rats by increasing autophagic activity and reducing oxidative damage, Mech. Ageing Dev., 134, 570, 10.1016/j.mad.2013.11.006 · DOI
  68. Zha, 2008, Genetic suppression of GH-IGF-1 activity, combined with lifelong caloric restriction, prevents age-related renal damage and prolongs the life span in rats, Am. J. Nephrol., 28, 755, 10.1159/000128607 · DOI
  69. Wang, 2019, Methionine restriction delays senescence and suppresses the senescence-associated secretory phenotype in the kidney through endogenous hydrogen sulfide, Cell cycle (Georgetown, Tex), 18, 1573, 10.1080/15384101.2019.1618124 · DOI
  70. Lee, 2018, Hydrogen sulfide ameliorates aging-associated changes in the kidney, Geroscience, 40, 163, 10.1007/s11357-018-0018-y · DOI
  71. Bitto, 2016, Transient rapamycin treatment can increase lifespan and healthspan in middle-aged mice, Elife, 5
  72. Andrikopoulos, 2019, The MEK inhibitor trametinib ameliorates kidney fibrosis by suppressing ERK1/2 and mTORC1 signaling, J. Am. Soc. Nephrol., 30, 33, 10.1681/ASN.2018020209 · DOI
  73. Yang, 2011, Cells derived from young bone marrow alleviate renal aging, J. Am. Soc. Nephrol., 22, 2028, 10.1681/ASN.2010090982 · DOI
  74. Hickson, 2016, Challenges and opportunities for stem cell therapy in patients with chronic kidney disease, Kidney Int., 89, 767, 10.1016/j.kint.2015.11.023 · DOI
  75. Eirin, 2013, Endothelial outgrowth cells shift macrophage phenotype and improve kidney viability in swine renal artery stenosis, Arterioscler. Thromb. Vasc. Biol., 33, 1006, 10.1161/ATVBAHA.113.301164 · DOI
  76. Rodriguez-Vita, 2017, Notch1 induces endothelial senescence and promotes tumor progression, Cell Cycle, 16, 911, 10.1080/15384101.2017.1316575 · DOI
  77. Sörensen-Zender, 2014, Renal tubular Notch signaling triggers a prosenescent state after acute kidney injury, Am. J. Physiol. Renal Physiol., 306, F907, 10.1152/ajprenal.00030.2014 · DOI
  78. Castellano, 2019, Complement component C5a induces aberrant epigenetic modifications in renal tubular epithelial cells accelerating senescence by Wnt4/βcatenin signaling after ischemia/reperfusion injury, Aging, 11, 4382, 10.18632/aging.102059 · DOI

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Metadata

Authors
Wang, Y., Wang, Y., Yang, M., & Ma, X.
Venue
Biomedicine & Pharmacotherapy
Publisher
Elsevier BV
Published
2021-03
Volume
135
Pages
111191
ISSN
0753-3322
DOI
10.1016/j.biopha.2020.111191
Cited by
34
References
40
Language
en
Licence
Funders
National Natural Science Foundation of China (81200596)

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