[1] Fiorentino M, Grandaliano G, Gesualdo L, et al. Acute kidney injury to chronic kidney disease transition[J]. Contrib Nephrol, 2018, 193: 45-54. [2] Hoste EaJ, Kellum JA, Selby NM, et al. Global epidemiology and outcomes of acute kidney injury[J]. Nat Rev Nephrol, 2018, 14: 607-625. [3] Santos RPD, Carvalho ARS, Peres LaB, et al. An epidemiologic overview of acute kidney injury in intensive care units[J]. Rev Assoc Med Bras (1992), 2019, 65: 1094-1101. [4] Coca SG, Singanamala S, Parikh CR. Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis[J]. Kidney Int, 2012, 81: 442-448. [5] Selby NM, Taal MW. Long-term outcomes after AKI-a major unmet clinical need[J]. Kidney Int, 2019, 95: 21-23. [6] Venkatachalam MA, Weinberg JM, Kriz W, et al. Failed tubule recovery, AKI-CKD transition, and kidney disease progression[J]. J Am Soc Nephrol, 2015, 26: 1765-1776. [7] Shu S, Zhu J, Liu Z, et al. Endoplasmic reticulum stress is activated in post-ischemic kidneys to promote chronic kidney disease[J]. E Bio Medicine, 2018, 37: 269-280. [8] Guzzi F, Cirillo L, Roperto RM, et al. Molecular mechanisms of the acute kidney injury to chronic kidney disease transition: an updated view[J]. Int J Mol Sci, 2019, 20.doi:10.3390/ijms20194941. [9] Franzin R, Stasi A, Fiorentino M, et al. Inflammaging and complement system: a link between acute kidney injury and chronic graft damage[J]. Front Immunol, 2020, 11.doi:10.3389/fimmu.2020.00734. [10] Black LM, Lever JM, Traylor AM, et al. Divergent effects of AKI to CKD models on inflammation and fibrosis[J]. Am J Physiol Renal Physiol, 2018, 315: F1107-F1118. [11] Chou YH, Huang TM, Pan SY, et al. Renin-angiotensin system inhibitor is associated with lower risk of ensuing chronic kidney disease after functional recovery from acute kidney injury[J]. Sci Rep, 2017, 7.doi:10.1038/srep46518. [12] Su H, Ye C, Lei CT, et al. Subcellular trafficking of tubular MDM2 implicates in acute kidney injury to chronic kidney disease transition during multiple low-dose cisplatin exposure[J]. FASEB J, 2020, 34: 1620-1636. [13] Szeto HH, Liu S, Soong Y, et al. Mitochondria protection after acute ischemia prevents prolonged upregulation of IL-1beta and IL-18 and arrests CKD[J]. J Am Soc Nephrol, 2017, 28: 1437-1449. [14] Bataille A, Galichon P, Chelghoum N, et al. Increased fatty acid oxidation in differentiated proximal tubular cells surviving a reversible episode of acute kidney injury[J]. Cell Physiol Biochem, 2018, 47: 1338-1351. [15] Chen DQ, Feng YL, Chen L, et al. Poricoic acid A enhances melatonin inhibition of AKI-to-CKD transition by regulating Gas6/AxlNFkappaB/Nrf2 axis[J]. Free Radic Biol Med, 2019, 134: 484-497. [16] Skrypnyk NI, Voziyan P, Yang H, et al. Pyridoxamine reduces postinjury fibrosis and improves functional recovery after acute kidney injury[J]. Am J Physiol Renal Physiol, 2016, 311: F268-277. [17] Liu Q, Zhang D, Hu D, et al. The role of mitochondria in NLRP3 inflammasome activation[J]. Mol Immunol, 2018, 103: 115-124. [18] Maekawa H, Inagi R. Pathophysiological role of organelle stress/crosstalk in AKI-to-CKD Transition[J]. Semin Nephrol, 2019, 39: 581-588. [19] Yang H, Li R, Zhang L, et al. p53-cyclophilin D mediates renal tubular cell apoptosis in ischemia-reperfusion-induced acute kidney injury[J]. Am J Physiol Renal Physiol, 2019, 317: F1311-F1317. [20] Zhao JY, Wang XL, Yang YC, et al. Upregulated miR-101 inhibits acute kidney injury-chronic kidney disease transition by regulating epithelial-mesenchymal transition[J]. Hum Exp Toxicol, 2020.doi:10.1177/0960327120937334. [21] Zhao L, Han F, Wang J, et al. Current understanding of the administration of mesenchymal stem cells in acute kidney injury to chronic kidney disease transition: a review with a focus on preclinical models[J]. Stem Cell Res Ther, 2019, 10.doi:10.1186/s13287-019-1507-3. [22] Gao L, Zhong X, Jin J, et al. Potential targeted therapy and diagnosis based on novel insight into growth factors, receptors, and downstream effectors in acute kidney injury and acute kidney injury-chronic kidney disease progression[J]. Signal Transduct Target Ther, 2020, 5.doi:10.1038/s41392-020-0106-1. [23] Aparicio-Trejo OE, Avila-Rojas SH, Tapia E, et al. Chronic impairment of mitochondrial bioenergetics and beta-oxidation promotes experimental AKI-to-CKD transi-tion induced by folic acid[J]. Free Radic Biol Med, 2020, 154: 18-32. [24] Zhang W, Sha Y, Wei K, et al. Rotenone ameliorates chronic renal injury caused by acute ischemia/reperfusion[J]. Oncotarget, 2018, 9: 24199-24208. |