Mitochondrial DNA may act as a biomarker to predict donor-kidney quality.


Journal

Clinical transplantation
ISSN: 1399-0012
Titre abrégé: Clin Transplant
Pays: Denmark
ID NLM: 8710240

Informations de publication

Date de publication:
11 2021
Historique:
revised: 13 08 2021
received: 02 02 2021
accepted: 18 08 2021
pubmed: 28 8 2021
medline: 3 2 2022
entrez: 27 8 2021
Statut: ppublish

Résumé

Kidney transplantation is the best therapy for end-stage renal disease. Demand for kidney transplantation rises year-on-year, and the gap between kidney supply and demand remains large. To meet this clinical need, a gradual expansion in the supply of donors is required. However, clinics lack appropriate tools capable of quickly and accurately predicting post-transplant renal allograft function, and thus assess donor-kidney quality before transplantation. Mitochondrial DNA (mtDNA) is a key component of damage-associated molecular patterns (DAMPs) and plays an important part in ischemia-reperfusion injury (IRI), accelerating the progression of IRI by inducing inflammation and type I interferon responses. mtDNA is known to be closely involved in delayed graft function (DGF) and acute kidney injury (AKI) after transplantation. Thus, mtDNA is a potential biomarker able to predict post-transplant renal allograft function. This review summarizes mtDNA biology, the role mtDNA plays in renal transplantation, outlines advances in detecting mtDNA, and details mtDNA's able to predict post-transplant renal allograft function. We aim to elucidate the potential value of mtDNA as a biomarker in the prediction of IRI, and eventually provide help for predicting donor-kidney quality.

Identifiants

pubmed: 34448256
doi: 10.1111/ctr.14469
doi:

Substances chimiques

Biomarkers 0
DNA, Mitochondrial 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

e14469

Informations de copyright

© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Références

Wolfe RA, Ashby VB, Milford EL, et al. Comparison of mortality in all patients on dialysis, patients on dialysis awaiting transplantation, and recipients of a first cadaveric transplant %. N Engl J Med. 1999;341(23):1725-1730.
Perico N, Codreanu I, Schieppati A, Remuzzi G. The future of renoprotection. Kidney Int Suppl. 2005(97):S95-101.
Querard AH, Foucher Y, Combescure C, et al. Comparison of survival outcomes between expanded criteria donor and standard criteria donor kidney transplant recipients: a systematic review and meta-analysis. Transpl Int. 2016;29(4):403-415.
Bellomo R, Kellum JA, Ronco C. Defining acute renal failure: physiological principles. Intensive Care Med. 2004;30(1):33-37.
Reese PP, Hall IE, Weng FL, et al. Associations between deceased-donor urine injury biomarkers and kidney transplant outcomes. J Am Soc Nephrol. 2016;27(5):1534-1543.
Kim K, Moon H, Lee YH, et al. Clinical relevance of cell-free mitochondrial DNA during the early postoperative period in kidney transplant recipients. Sci Rep. 2019;9(1):18607.
Han F, Wan S, Sun Q, et al. Donor plasma mitochondrial dna is correlated with posttransplant renal allograft function. Transplantation. 2019;103(11):2347-2358.
Nass S, Nass MM, Hennix U. Deoxyribonucleic Acid in Isolated Rat-Liver Mitochondria. Biochim Biophys Acta. 1965;95:426-435.
Shadel GS, Clayton DA. Mitochondrial DNA maintenance in vertebrates. Annu Rev Biochem. 1997;66:409-435.
Galluzzi L, Kepp O, Kroemer G. Mitochondria: master regulators of danger signalling. Nat Rev Mol Cell Biol. 2012;13(12):780-788.
Fang C, Wei X, Wei Y. Mitochondrial DNA in the regulation of innate immune responses. Protein Cell. 2016;7(1):11-16.
Lee SR, Han J. Mitochondrial nucleoid: shield and switch of the mitochondrial genome. Oxid Med Cell Longev. 2017;2017:8060949.
Kolesnikov AA. The mitochondrial genome. The nucleoid. Biochemistry (Mosc). 2016;81(10):1057-1065.
Hu Q, Zhou Q, Wu J, Wu X, Ren J. The role of mitochondrial DNA in the development of ischemia reperfusion injury. Shock. 2019;51(1):52-59.
Dhanwani R, Takahashi M, Sharma S. Cytosolic sensing of immuno-stimulatory DNA, the enemy within. Curr Opin Immunol. 2018;50:82-87.
Guo Z, Yu S, Chen X, Ye R, Zhu W, Liu X. NLRP3 is involved in ischemia/reperfusion injury. CNS Neurol Disord Drug Targets. 2016;15(6):699-712.
Cavaille-Coll M, Bala S, Velidedeoglu E, et al. Summary of FDA workshop on ischemia reperfusion injury in kidney transplantation. Am J Transplant. 2013;13(5):1134-1148.
Shoskes DA, Halloran PF. Delayed graft function in renal transplantation: etiology, management and long-term significance. J Urol. 1996;155(6):1831-1840.
Menon MC, Banu K. Circulating donor mitochondrial DNA: tales the dead may tell. Transplantation. 2019;103(11):2217-2218.
Afrifa J, Zhao T, Yu J. Circulating mitochondria DNA, a non-invasive cancer diagnostic biomarker candidate. Mitochondrion. 2019;47:238-243.
Bae JH, Jo SI, Kim SJ, et al. Circulating cell-free mtDNA contributes to AIM2 inflammasome-mediated chronic inflammation in patients with type 2 diabetes. Cells. 2019;8(4).
Caielli S, Athale S, Domic B, et al. Oxidized mitochondrial nucleoids released by neutrophils drive type I interferon production in human lupus. J Exp Med. 2016;213(5):697-713.
Silzer T, Barber R, Sun J, et al. Circulating mitochondrial DNA: new indices of type 2 diabetes-related cognitive impairment in Mexican Americans. PLoS One. 2019;14(3):e0213527.
Oka T, Hikoso S, Yamaguchi O, et al. Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure. Nature. 2012;485(7397):251-255.
Garcia-Martinez I, Santoro N, Chen Y, et al. Hepatocyte mitochondrial DNA drives nonalcoholic steatohepatitis by activation of TLR9. J Clin Invest. 2016;126(3):859-864.
Kim J, Gupta R, Blanco LP, et al. VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease. Science. 2019;366(6472):1531-1536.
Bernardi P, Why F-ATP. Synthase remains a strong candidate as the mitochondrial permeability transition pore. Front Physiol. 2018;9:1543.
Bernardi P, Di LisaF. The mitochondrial permeability transition pore: molecular nature and role as a target in cardioprotection. J Mol Cell Cardiol. 2015;78:100-106.
Gutierrez-Aguilar M, Baines CP. Structural mechanisms of cyclophilin D-dependent control of the mitochondrial permeability transition pore. Biochim Biophys Acta. 2015;1850(10):2041-2047.
Giorgio V, Guo L, Bassot C, Petronilli V, Bernardi P. Calcium and regulation of the mitochondrial permeability transition. Cell Calcium. 2018;70:56-63.
Bernardi P, Rasola A, Forte M, Lippe G. The mitochondrial permeability transition pore: channel formation by F-ATP synthase, integration in signal transduction, and role in pathophysiology. Physiol Rev. 2015;95(4):1111-1155.
Perez-Trevino P, Velasquez M, Garcia N. Mechanisms of mitochondrial DNA escape and its relationship with different metabolic diseases. Biochim Biophys Acta Mol Basis Dis. 2020;1866(6):165761.
Koulintchenko M, Temperley RJ, Mason PA, Dietrich A, Lightowlers RN. Natural competence of mammalian mitochondria allows the molecular investigation of mitochondrial gene expression. Hum Mol Genet. 2006;15(1):143-154.
Szabo I, Bathori G, Tombola F, et al. Double-stranded DNA can be translocated across a planar membrane containing purified mitochondrial porin. FASEB J. 1998;12(6):495-502.
West AP, Shadel GS. Mitochondrial DNA in innate immune responses and inflammatory pathology. Nat Rev Immunol. 2017;17(6):363-375.
Ding Z, Liu S, Wang X, et al. LOX-1, mtDNA damage, and NLRP3 inflammasome activation in macrophages: implications in atherogenesis. Cardiovasc Res. 2014;103(4):619-628.
Ding Z, Liu S, Wang X, Khaidakov M, Dai Y, Mehta JL. Oxidant stress in mitochondrial DNA damage, autophagy and inflammation in atherosclerosis. Sci Rep. 2013;3:1077.
Nakahira K, Haspel JA, Rathinam VA, et al. Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome. Nat Immunol. 2011;12(3):222-230.
Sliter DA, Martinez J, Hao L, et al. Parkin and PINK1 mitigate STING-induced inflammation. Nature. 2018;561(7722):258-262.
White MJ, McArthur K, Metcalf D, et al. Apoptotic caspases suppress mtDNA-induced STING-mediated type I IFN production. Cell. 2014;159(7):1549-1562.
Wei Q, Dong G, Chen JK, Ramesh G, Dong Z. Bax and Bak have critical roles in ischemic acute kidney injury in global and proximal tubule-specific knockout mouse models. Kidney Int. 2013;84(1):138-148.
Lin JY, Jing R, Lin F, Ge WY, Dai HJ, Pan L. High tidal volume induces mitochondria damage and releases mitochondrial DNA to aggravate the ventilator-induced lung injury. Front Immunol. 2018;9:1477.
Liu R, Xu F, Bi S, Zhao X, Jia B, Cen Y. Mitochondrial DNA-induced inflammatory responses and lung injury in thermal injury murine model: protective effect of cyclosporine-A. J Burn Care Res. 2019;40(3):355-360.
Xiao Z, Jia B, Zhao X, Bi S, Meng W. Attenuation of lipopolysaccharide-induced acute lung injury by cyclosporine-A via suppression of mitochondrial DNA. Med Sci Monit. 2018;24:7682-7688.
Aswani A, Manson J, Itagaki K, et al. Scavenging circulating mitochondrial DNA as a potential therapeutic option for multiple organ dysfunction in trauma hemorrhage. Front Immunol. 2018;9:891.
Hajizadeh S, DeGroot J, TeKoppele JM, Tarkowski A, Collins LV. Extracellular mitochondrial DNA and oxidatively damaged DNA in synovial fluid of patients with rheumatoid arthritis. Arthritis Res Ther. 2003;5(5):R234-240.
Marques PE, Amaral SS, Pires DA, et al. Chemokines and mitochondrial products activate neutrophils to amplify organ injury during mouse acute liver failure. Hepatology. 2012;56(5):1971-1982.
Thurairajah K, Briggs GD, Balogh ZJ. The source of cell-free mitochondrial DNA in trauma and potential therapeutic strategies. Eur J Trauma Emerg Surg. 2018;44(3):325-334.
Wang L, Xie L, Zhang Q, et al. Plasma nuclear and mitochondrial DNA levels in acute myocardial infarction patients. Coron Artery Dis. 2015;26(4):296-300.
Wu L, Xu W, Wang F, Lv T, Yin Z, Song Y. Plasma mtDNA analysis aids in predicting pancreatic necrosis in acute pancreatitis patients: a pilot study. Dig Dis Sci. 2018;63(11):2975-2982.
Shimada K, Crother TR, Karlin J, et al. Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. Immunity. 2012;36(3):401-414.
Fann DY, Lee SY, Manzanero S, Chunduri P, Sobey CG, Arumugam TV. Pathogenesis of acute stroke and the role of inflammasomes. Ageing Res Rev. 2013;12(4):941-966.
Tumurkhuu G, Shimada K, Dagvadorj J, et al. Ogg1-dependent DNA repair regulates NLRP3 inflammasome and prevents atherosclerosis. Circ Res. 2016;119(6):e76-90.
Liu L, Yang M, Kang R, et al. HMGB1-DNA complex-induced autophagy limits AIM2 inflammasome activation through RAGE. Biochem Biophys Res Commun. 2014;450(1):851-856.
Jabir MS, Hopkins L, Ritchie ND, et al. Mitochondrial damage contributes to Pseudomonas aeruginosa activation of the inflammasome and is downregulated by autophagy. Autophagy. 2015;11(1):166-182.
Kawasaki T, Kawai T. Toll-like receptor signaling pathways. Front Immunol. 2014;5:461.
Castellaneta A, Yoshida O, Kimura S, et al. Plasmacytoid dendritic cell-derived IFN-alpha promotes murine liver ischemia/reperfusion injury by induction of hepatocyte IRF-1. Hepatology. 2014;60(1):267-277.
Zhang M, Downes CE, Wong CHY, et al. Type-I interferon signalling through IFNAR1 plays a deleterious role in the outcome after stroke. Neurochem Int. 2017;108:472-480.
Zhai Y, Qiao B, Gao F, et al. Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Hepatology. 2008;47(1):199-206.
!!! INVALID CITATION !!! [60].
McArthur K, Whitehead LW, Heddleston JM, et al. BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis. Science. 2018;359(6378).
Riley JS, Quarato G, Cloix C, et al. Mitochondrial inner membrane permeabilisation enables mtDNA release during apoptosis. EMBO J. 2018;37(17).
Gao D, Wu J, Wu YT, et al. Cyclic GMP-AMP synthase is an innate immune sensor of HIV and other retroviruses. Science. 2013;341(6148):903-906.
Chen Q, Sun L, Chen ZJ. Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat Immunol. 2016;17(10):1142-1149.
Storek KM, Gertsvolf NA, Ohlson MB, Monack DM. cGAS and Ifi204 cooperate to produce type I IFNs in response to Francisella infection. J Immunol. 2015;194(7):3236-3245.
Pazmandi K, Agod Z, Kumar BV, et al. Oxidative modification enhances the immunostimulatory effects of extracellular mitochondrial DNA on plasmacytoid dendritic cells. Free Radic Biol Med. 2014;77:281-290.
Mallavia B, Liu F, Lefrancais E, et al. Mitochondrial DNA stimulates TLR9-dependent neutrophil extracellular trap formation in primary graft dysfunction. Am J Respir Cell Mol Biol. 2020;62(3):364-372.
Tullius SG, Milford E. Kidney allocation and the aging immune response. N Engl J Med. 2011;364(14):1369-1370.
Oberhuber R, Heinbokel T, Cetina Biefer HR, et al. CD11c+ dendritic cells accelerate the rejection of older cardiac transplants via Interleukin-17A. Circulation. 2015;132(2):122-131.
Tullius SG, Rabb H. Improving the supply and quality of deceased-donor organs for transplantation. N Engl J Med. 2018;378(20):1920-1929.
Tullius SG, Reutzel-Selke A, Egermann F, et al. Contribution of prolonged ischemia and donor age to chronic renal allograft dysfunction. J Am Soc Nephrol. 2000;11(7):1317-1324.
Iske J, Seyda M, Heinbokel T, et al. Senolytics prevent mt-DNA-induced inflammation and promote the survival of aged organs following transplantation. Nat Commun. 2020;11(1):4289.
Jansen MPB, Pulskens WPC, Uil M, et al. Urinary mitochondrial DNA associates with delayed graft function following renal transplantation. Nephrol Dial Transplant. 2020;35(8):1320-1327.
Whitaker RM, Stallons LJ, Kneff JE, et al. Urinary mitochondrial DNA is a biomarker of mitochondrial disruption and renal dysfunction in acute kidney injury. Kidney Int. 2015;88(6):1336-1344.
Tin A, Grams ME, Ashar FN, et al. Association between mitochondrial DNA copy number in peripheral blood and incident CKD in the atherosclerosis risk in communities study. J Am Soc Nephrol. 2016;27(8):2467-2473.
Rao M, Li L, Demello C, et al. Mitochondrial DNA injury and mortality in hemodialysis patients. J Am Soc Nephrol. 2009;20(1):189-196.
Lim PS, Cheng YM, Wei YH. Large-scale mitochondrial DNA deletions in skeletal muscle of patients with end-stage renal disease. Free Radic Biol Med. 2000;29(5):454-463.
Lim PS, Ma YS, Cheng YM, et al. Mitochondrial DNA mutations and oxidative damage in skeletal muscle of patients with chronic uremia. J Biomed Sci. 2002;9(6 Pt 1):549-560.
Ashar FN, Zhang Y, Longchamps RJ, et al. Association of mitochondrial DNA copy number with cardiovascular disease. JAMA Cardiol. 2017;2(11):1247-1255.
Zhang Y, Guallar E, Ashar FN, et al. Association between mitochondrial DNA copy number and sudden cardiac death: findings from the Atherosclerosis Risk in Communities study (ARIC). Eur Heart J. 2017;38(46):3443-3448.
Sun L, Xie P, Wada J, et al. Rap1b GTPase ameliorates glucose-induced mitochondrial dysfunction. J Am Soc Nephrol. 2008;19(12):2293-2301.
Sarafidis PA, Stafylas PC, Georgianos PI, Saratzis AN, Lasaridis AN. Effect of thiazolidinediones on albuminuria and proteinuria in diabetes: a meta-analysis. Am J Kidney Dis. 2010;55(5):835-847.
Eirin A, Ebrahimi B, Zhang X, et al. Mitochondrial protection restores renal function in swine atherosclerotic renovascular disease. Cardiovasc Res. 2014;103(4):461-472.
Zhan M, Usman IM, Sun L, Kanwar YS. Disruption of renal tubular mitochondrial quality control by Myo-inositol oxygenase in diabetic kidney disease. J Am Soc Nephrol. 2015;26(6):1304-1321.

Auteurs

Changzhen Hao (C)

Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Institute of Urology, Capital Medical University, Beijing, China.

Jiandong Zhang (J)

Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Institute of Urology, Capital Medical University, Beijing, China.

Feilong Zhang (F)

Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Institute of Urology, Capital Medical University, Beijing, China.

Jiyue Wu (J)

Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Institute of Urology, Capital Medical University, Beijing, China.

Huawei Cao (H)

Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Institute of Urology, Capital Medical University, Beijing, China.

Wei Wang (W)

Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Institute of Urology, Capital Medical University, Beijing, China.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH