|
|
|
|
|
The research progress of mitochondrial dynamics in acute kidney injury |
Long Rui-ting, Xu Fang, Liao Xiao-hui |
Department of Nephrology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China |
|
|
Abstract Mitochondria are a class of highly dynamic organelles. Under physiological conditions, the two processes of fission and fusion continue to maintain the mitochondrial morphology and cell homeostasis.In recent years,numerous studies have observed changes in mitochondrial dynamics during acute kidney injury.However, its role in the development of the disease and the mechanism has not been fully understood. This review summarizes the recent advances in mitochondrial dynamics and acute kidney injury, which helps to understand the pathogenesis of acute kidney injury and lay the foundation for seeking new therapeutic strategies.
|
|
Corresponding Authors:
Liao Xiao-hui, E-mail: lxheducation@163.com
|
|
|
|
[1]Mehta RL, Cerdá J, Burdmann EA, et al. International Society of Nephrology′s 0by25 initiative for acute kidney injury (zero preventable deaths by 2025): a human rights case for nephrology[J]. Lancet, 2015, 385(9987):2616-2643.
[2]Kaddourah A, Basu RK, Bagshaw SM, et al. Epidemiology of Acute Kidney Injury in Critically Ill Children and Young Adults[J]. N Engl J Med, 2017, 376(1):11-20.
[3]Leung KC, Tonelli M, James MT. Chronic kidney disease following acute kidney injury-risk and outcomes[J]. Nat Rev Nephrol, 2013, 9(2):77-85.
[4]Ishihara N, Otera H, Oka T, et al. Regulation and physiologic functions of GTPases in mitochondrial fusion and fission inmammals[J].Antioxid Redox Signal, 2013, 19(4):389-399.
[5]Ishimoto Y, Inagi R. Mitochondria: a therapeutic target in acute kidney injury[J]. Nephrol Dial Transplant, 2016, 31(7):1062-1069.
[6]Zhan M, Brooks C, Liu F, et al. Mitochondrial dynamics: regulatory mechanisms and emerging role in renal pathophysiology[J]. Kidney Int, 2013, 83(4):568-581.
[7]Lee H, Smith SB, Yoon Y. The short variant of the mitochondrial dynamin OPA1 maintains mitochondrial energetics and cristae structure[J]. J Biol Chem, 2017, 292(17):7115-7130.
[8]Macdonald PJ, Francy CA, Stepanyants N, et al. Distinct Splice Variants of Dynamin-related Protein 1 Differentially Utilize Mitochondrial Fission Factor as an Effector of Cooperative GTPase Activity[J]. J Biol Chem, 2016, 291(1):493-507.
[9]Bhargava P, Schnellmann RG. Mitochondrial energetics in the kidney[J]. Nat Rev Nephrol, 2017, 13(10):629-646.
[10]Brooks C, Wei Q, Cho SG, et al. Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models[J]. J Clin Invest, 2009, 119(5):1275-1285.
[11]Noh MR, Kim KY, Han SJ, et al. Methionine Sulfoxide Reductase A Deficiency Exacerbates Cisplatin-Induced Nephrotoxicity via Increased Mitochondrial Damage and Renal Cell Death[J]. Antioxid Redox Signal, 2017, 27(11):727-741.
[12]Funk JA, Schnellmann RG. Persistent disruption of mitochondrial homeostasis after acute kidney injury[J]. Am J Physiol Renal Physiol, 2012, 302(7):F853-864.
[13]Tang WX, Wu WH, Qiu HY, et al. Amelioration of rhabdomyolysis-induced renal mitochondrial injury and apoptosis through suppression of Drp-1 translocation[J]. J Nephrol, 2013, 26(6):1073-1082.
[14]Cho SG, Du Q, Huang S, et al. Drp1 dephosphorylation in ATP depletion-induced mitochondrial injury and tubular cell apoptosis[J]. Am J Physiol Renal Physiol, 2010, 299(1):F199-206.
[15]Perry HM, Huang L, Wilson RJ, et al. Dynamin-Related Protein 1 Deficiency PromotesRecovery from AKI[J]. J Am Soc Nephrol, 2018, 29(1):194-206.
[16]Xiao X, Hu Y, Quirós PM, et al. OMA1 mediates OPA1 proteolysis and mitochondrial fragmentation in experimental models of ischemic kidney injury[J]. Am J Physiol Renal Physiol, 2014, 306(11):F1318-1326.
[17]Aung LHH, Li R, Prabhakar BS, et al. Knockdown of Mtfp1 can minimize doxorubicin cardiotoxicity by inhibiting Dnm1l-mediated mitochondrial fission[J]. J Cell Mol Med, 2017, 21(12):3394-3404.
[18]Morita M, Prudent J, Basu K, et al. mTOR Controls Mitochondrial Dynamics and Cell Survival via MTFP1[J]. Mol Cell, 2017, 67(6):922-935. |
|
|
|