[1] |
张百红,岳红云. 肿瘤检查点相关研究进展[J]. 癌症进展,2015, 13(3):260-264.
|
[2] |
Reinhardt HC, Yaffe MB. Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2 [J]. Curr Opin Cell Biol, 2009, 21(2): 245-255.
|
[3] |
Griffin SV, Pichler R, Dittrich M, et al. Cell cycle control in glomerular disease [J]. Springer Semin Immunopathol, 2003, 24(4): 441-457.
|
[4] |
Wang J, Li Q, Yuan J, et al. CDK4/6 inhibitor-SHR6390 exerts potent antitumor activity in esophageal squamous cell carcinoma by inhibiting phosphorylated Rb and inducing G1 cell cycle arrest [J]. J Transl Med, 2017, 15(1): 127.
|
[5] |
Osorio J. Cell cycle: repurposing MYC and E2F in the absence of RB [J]. Nat Rev Mol Cell Biol, 2015, 16(9): 516-517.
|
[6] |
Feng C, Yang M, Zhang Y, et al. Cyclic mechanical tension reinforces DNA damage and activates the p53-p21-Rb pathway to induce premature senescence of nucleus pulposus cells [J]. Int J Mol Med, 2018, 41(6): 3316-3326.
|
[7] |
Wu CF, Chiang WC, Lai CF, et al. Transforming growth factor beta-1 stimulates profibrotic epithelial signaling to activate pericyte-myofibroblast transition in obstructive kidney fibrosis [J]. Am J Pathol, 2013, 182(1): 118-113.
|
[8] |
Verduzco D, Dovey JS, Shukla AA, et al. Multiple isoforms of CDC25 oppose ATM activity to maintain cell proliferation during vertebrate development [J]. Mol Cancer Res, 2012, 10(11): 1451-1461.
|
[9] |
Boutros R, Dozier C, Ducommun B. The when and wheres of CDC25 phosphatases [J]. Curr Opin Cell Biol, 2006, 18(2): 185-191.
|
[10] |
Lin JS, Susztak K. Podocytes: the weakest link in diabetic kidney disease [J]. Curr Diab Rep, 2016, 16(5): 45.
|
[11] |
Wolf G, Chen S, Ziyadeh FN. From the periphery of the glomerular capillary wall toward the center of disease: podocyte injury comes of age in diabetic nephropathy [J]. Diabetes, 2005, 54(6): 1626-1634.
|
[12] |
Steffes MW, Schmidt D, McCrery R, et al. Glomerular cell number in normal subjects and in type 1 diabetic patients [J]. Kidney Int, 2001, 59(6): 2104-2113.
|
[13] |
Vitale I, Galluzzi L, Castedo M, et al. Mitotic catastrophe: a mechanism for avoiding genomic instability [J]. Nat Rev Mol Cell Biol, 2011, 12(6): 385-392.
|
[14] |
Vakifahmetoglu H, Olsson M, Zhivotovsky B. Death through a tragedy: mitotic catastrophe [J]. Cell Death Differ, 2008, 15(7): 1153-1162.
|
[15] |
Tang H, Lei CT, Ye C, et al. MDM2 is implicated in high-glucose-induced podocyte mitotic catastrophe via Notch1 signalling [J]. J Cell Mol Med, 2017, 21(12): 3435-3444.
|
[16] |
Migliorini A, Angelotti ML, Mulay SR, et al. The antiviral cytokines IFN-alpha and IFNbeta modulate parietal epithelial cells and promote podocyte loss: implications for IFN toxicity, viral glomerulonephritis, and glomerular regeneration [J]. Am J Pathol, 2013, 183(2): 431-440.
|
[17] |
Mulay SR, Thomasova D, Ryu M, et al. Podocyte loss involves MDM2-driven mitotic catastrophe [J]. J Pathol, 2013, 230(3): 322-335.
|
[18] |
Price PM. A role for novel cell-cycle proteins in podocyte biology [J]. Kidney Int, 2010, 77(8): 660-661.
|
[19] |
Barisoni L, Mokrzycki M, Sablay L, et al. Podocyte cell cycle regulation and proliferation in collapsing glomerulopathies [J]. Kidney Int, 2000, 58(1): 137-143.
|
[20] |
Liapis H, Romagnani P, Anders HJ. New insights into the pathology of podocyte loss: mitotic catastrophe [J]. Am J Pathol, 2013, 183(5): 1364-1374.
|
[21] |
Kriz W, Lemley KV. A potential role for mechanical forces in the detachment of podocytes and the progression of CKD [J]. J Am Soc Nephrol, 2015, 26(2): 258-269.
|
[22] |
Hara M, Oohara K, Dai DF, et al. Mitotic catastrophe causes podocyte loss in the urine of human diabetics [J]. Am J Pathol, 2019, 189(2): 248-257.
|
[23] |
Lasagni L, Lazzeri E, Shankland SJ, et al. Podocyte mitosis-a catastrophe [J]. Curr Mol Med, 2013, 13(1): 13-23.
|
[24] |
Hagen M, Pfister E, Kosel A, et al. Cell cycle re-entry sensitizes podocytes to injury induced death [J]. Cell Cycle, 2016, 15(14): 1929-1937.
|
[25] |
Hoshi S, Shu Y, Yoshida F, et al. Podocyte injury promotes progressive nephropathy in zucker diabetic fatty rats [J]. Lab Invest, 2002, 82(1): 25-35.
|
[26] |
Baba M, Wada J, Eguchi J, et al. Galectin-9 inhibits glomerular hypertrophy in db/db diabetic mice via cell-cycle-dependent mechanisms [J]. J Am Soc Nephrol, 2005, 16(11): 3222-3234.
|
[27] |
Marshall CB, Krofft RD, Pippin JW, et al. CDK inhibitor p21 is prosurvival in adriamycin-induced podocyte injury, in vitro and in vivo [J]. Am J Physiol Renal Physiol, 2010, 298(5): F1140-F1151.
|
[28] |
Sun T, Mu D, Cui J. Mathematical model identifies effective P53 accumulation with target gene binding affinity in DNA damage response for cell fate decision [J]. Cell Cycle, 2018, 17(24): 2716-2730.
|
[29] |
Wu D, Prives C. Relevance of the p53-MDM2 axis to aging [J]. Cell Death Differ, 2018, 25(1): 169-179.
|
[30] |
Liu L, Charville GW, Cheung TH, et al. Impaired Notch signaling leads to a decrease in p53 activity and mitotic catastrophe in aged muscle stem cells [J]. Cell Stem Cell, 2018, 23(4): 544-556.
|
[31] |
Zhao K, Yang Y, Zhang G, et al. Regulation of the Mdm2-p53 pathway by the ubiquitin E3 ligase MARCH7 [J]. EMBO Rep, 2018, 19(2): 305-319.
|
[32] |
Thomasova D, Mulay SR, Bruns H, et al. p53-independent roles of MDM2 in NF-kappaB signaling: implications for cancer therapy, wound healing, and autoimmune diseases [J]. Neoplasia, 2012, 14(12): 1097-1101.
|
[33] |
Hilliard S, Aboudehen K, Yao X, et al. Tight regulation of p53 activity by Mdm2 is required for ureteric bud growth and branching [J]. Dev Biol, 2011, 353(2): 354-366.
|
[34] |
Hilliard SA, Yao X, El-Dahr SS. Mdm2 is required for maintenance of the nephrogenic niche [J]. Dev Biol, 2014, 387(1): 1-14.
|
[35] |
Ronconi E, Sagrinati C, Angelotti ML, et al. Regeneration of glomerular podocytes by human renal progenitors [J]. J Am Soc Nephrol, 2009, 20(2): 322-332.
|
[36] |
Wanner N, Hartleben B, Herbach N, et al. Unraveling the role of podocyte turnover in glomerular aging and injury [J]. J Am Soc Nephrol, 2014, 25(4): 707-716.
|
[37] |
Lasagni L, Ballerini L, Angelotti ML, et al. Notch activation differentially regulates renal progenitors proliferation and differentiation toward the podocyte lineage in glomerular disorders [J]. Stem Cells, 2010, 28(9): 1674-1685.
|
[38] |
Kostapanos MS, Liberopoulos EN, Elisaf MS. Statin pleiotropy against renal injury [J]. J Cardiometab Syndr, 2009, 4(1): E4-E9.
|
[39] |
Sakaguchi M, Isono M, Isshiki K, et al. Inhibition of mTOR signaling with rapamycin attenuates renal hypertrophy in the early diabetic mice [J]. Biochem Biophys Res Commun, 2006, 340(1): 296-301.
|
[40] |
Benigni A, Morigi M, Rizzo P, et al. Inhibiting angiotensin-converting enzyme promotes renal repair by limiting progenitor cell proliferation and restoring the glomerular architecture [J]. Am J Pathol, 2011, 179(2): 628-638.
|
[41] |
Obligado SH, Ibraghimov-Beskrovnaya O, Zuk A, et al. CDK/GSK-3 inhibitors as therapeutic agents for parenchymal renal diseases [J]. Kidney Int, 2008, 73(6): 684-690.
|
[42] |
周谊霞,杨文晴,李龙,等. GSK-3β抑制剂通过wnt/β-catenin调控OPG在DKD大鼠肾组织中作用 [J]. 中国公共卫生,2019, 35(6): 738-741.
|
[43] |
Canaud G, Bonventre JV. Cell cycle arrest and the evolution of chronic kidney disease from acute kidney injury [J]. Nephrol Dial Transplant, 2015, 30(4): 575-583.
|
[44] |
Donehower LA, Lozano G. 20 years studying p53 functions in genetically engineered mice [J]. Nat Rev Cancer, 2009, 9(11): 831-841.
|
[45] |
Christophorou MA, Ringshausen I, Finch AJ, et al. The pathological response to DNA damage does not contribute to p53-mediated tumour suppression [J]. Nature, 2006, 443(7108): 214-217.
|
[46] |
刘同阳,郭海强,朱美妍,等. 突变型p53与其合成致死基因的研究进展 [J]. 遗传,2015, 37(4): 321-326.
|