|
|
Research progress on ischemia-reperfusion injury of diabetic organs |
YI Haoran WANG Lei ZHU Hengcheng |
Department of Urology, Renmin Hospital of Wuhan University, Hubei Province, Wuhan 430060, China |
|
|
Abstract Diabetes is a high incidence of metabolic disorders, the patient′s blood sugar stayed high for a long time, cell damage is mediated by inflammatory response and oxidative stress. Ischemia-reperfusion injury (IRI) is a phenomenon that the injury of ischemic organs is further aggravated after the restoration of blood perfusion. It plays an important role in the pathophysiological mechanism of cerebral infarction, myocardial infarction, renal IRI, intestinal IRI and liver IRI. These are the leading causes of organ damage, including transplant failure, and even death. Recent studies have shown that diabetes can worsen IRI in organs. This paper reviews the research progress of IRI in major diabetic organs.
|
|
|
|
|
[1] Barzegar M,Kaur G,Gavins F,et al. Potential therapeutic roles of stem cells in ischemia-reperfusion injury [J]. Stem Cell Res,2019,37:101 421.
[2] Luitse MJ,Biessels GJ,Rutten GE,et al. Diabetes,hyperglycaemia,and acute ischaemic stroke [J]. Lancet Neurol,2012,11(3):261-271.
[3] Bragg F,Li L,Smith M,et al. Associations of blood glucose and prevalent diabetes with risk of cardiovascular disease in 500 000 adult Chinese:the China Kadoorie Biobank [J]. Diabet Med,2014,31(5):540-551.
[4] Thom T,Haase N,Rosamond W,et al. Heart disease and stroke statistics--2006 update:a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee [J]. Circulation,2006,113(6):e85-e151.
[5] Yu Q,Gao F,Ma XL. Insulin says NO to cardiovascular disease [J]. Cardiovasc Res,2011,89(3):516-524.
[6] Murarikova M,Ferko M,Waczulikova I,et al. Changes in mitochondrial properties may contribute to enhanced resistance to ischemia-reperfusion injury in the diabetic rat heart [J]. Can J Physiol Pharmacol,2017,95(8):969-976.
[7] Halestrap AP. A pore way to die:the role of mitochondria in reperfusion injury and cardioprotection [J]. Biochem Soc Trans,2010,38(4):841-860.
[8] Hausenloy DJ,Boston-Griffiths EA,Yellon DM. Cyclosporin A and cardioprotection:from investigative tool to therapeutic agent [J]. Br J Pharmacol,2012,165(5):1235-1245.
[9] Sharp WW,Fang YH,Han M,et al. Dynamin-related protein 1 (Drp1)-mediated diastolic dysfunction in myocardial ischemia-reperfusion injury:therapeutic benefits of Drp1 inhibition to reduce mitochondrial fission [J]. FASEB J,2014,28(1):316-326.
[10] Ding M,Dong Q,Liu Z,et al. Inhibition of dynamin-related protein 1 protects against myocardial ischemia-reperfusion injury in diabetic mice [J]. Cardiovasc Diabetol,2017,16(1):19.
[11] 刘中砥,林峥,李兴旺.依达拉奉对大鼠肠部分缺血再灌注后肝损伤保护作用的实验研究[J].安徽医学,2008,29(3):263-265,232.
[12] Yue S,Zhou HM,Zhu JJ,et al. Hyperglycemia and liver ischemia reperfusion injury:a role for the advanced glycation endproduct and its receptor pathway [J]. Am J Transplant,2015,15(11):2877-2887.
[13] Zeng S,Feirt N,Goldstein M,et al. Blockade of receptor for advanced glycation end product (RAGE)attenuates ischemia and reperfusion injury to the liver in mice [J]. Hepatology,2004,39(2):422-432.
[14] Zeng S,Dun H,Ippagunta N,et al. Receptor for advanced glycation end product (RAGE)-dependent modulation of early growth response-1 in hepatic ischemia/reperfusion injury [J]. J Hepatol,2009,50(5):929-936.
[15] Metz VV,Kojro E,Rat D,et al. Induction of RAGE shedding by activation of G protein-coupled receptors [J]. PLoS One,2012,7(7):e41 823.
[16] Arumugam T,Ramachandran V,Gomez SB,et al. S100P-derived RAGE antagonistic peptide reduces tumor growth and metastasis [J]. Clin Cancer Res,2012,18(16):4356-4364.
[17] Maisonneuve P,Agodoa L,Gellert R,et al. Distribution of primary renal diseases leading to end-stage renal failure in the United States,Europe,and Australia/New Ze-aland:results from an international comparative study [J]. Am J Kidney Dis,2000,35(1):157-165.
[18] Shi H,Patschan D,Epstein T,et al. Delayed recovery of renal regional blood flow in diabetic mice subjected to acute ischemic kidney injury [J]. Am J Physiol Renal Physiol,2007,293(5):F1512-F1517.
[19] Zhang Y,Hu F,Wen J,et al. Effects of sevoflurane on NF-small ka,CyrillicB and TNF-alpha expression in renal ischemia-reperfusion diabetic rats [J]. Inflamm Res,2017,66(10):901-910.
[20] Katzberg RW,Barrett BJ. Risk of iodinated contrast material--induced nephropathy with intravenous administration [J]. Radiology,2007,243(3):622-628.
[21] Devarajan P. Update on mechanisms of ischemic acute kidney injury [J]. J Am Soc Nephrol,2006,17(6):1503-1520.
[22] Jiang T,Tian F,Zheng H,et al. Nrf2 suppresses lupus nephritis through inhibition of oxidative injury and the NF-kappaB-mediated inflammatory response [J]. Kidney Int,2014,85(2):333-343.
[23] Zhang G,Zou X,Huang Y,et al. Mesenchymal Stromal Cell-Derived Extracellular Vesicles Protect Against Acute Kidney Injury Through Anti-Oxidation by Enhancing Nrf2/ARE Activation in Rats [J]. Kidney Blood Press Res,2016,41(2):119-128.
[24] Shi S,Lei S,Tang C,et al. Melatonin attenuates acute kidney ischemia/reperfusion injury in diabetic rats by activation of the SIRT1/Nrf2/HO-1 signaling pathway [J]. Biosci Rep,2019,39(1).
[25] Shen X,Hu B,Xu G,et al. Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3beta Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats [J]. Kidney Blood Press Res,2017,42(2):369-378.
[26] Zhang Y,Hu F,Wen J,et al. Effects of sevoflurane on NF-small ka,CyrillicB and TNF-alpha expression in renal ischemia-reperfusion diabetic rats [J]. Inflamm Res,2017,66(10):901-910.
[27] Bragg F,Holmes MV,Iona A,et al. Association Between Diabetes and Cause-Specific Mortality in Rural and Urban Areas of China [J]. JAMA,2017,317(3):280-289.
[28] Roquer J,Rodriguez-Campello A,Cuadrado-Godia E,et al. Ischemic stroke in prediabetic patients [J]. J Neurol,2014,261(10):1866-1870.
[29] Hu G,Jousilahti P,Sarti C,et al. The effect of diabetes and stroke at baseline and during follow-up on stroke mortality [J]. Diabetologia,2006,49(10):2309-2316.
[30] Lei C,Wu B,Cao T,et al. Activation of the high-mobility group box 1 protein-receptor for advanced glycation end-products signaling pathway in rats during neurogenesis after intracerebral hemorrhage [J]. Stroke,2015,46(2):500-506.
[31] Kwak MS,Lim M,Lee YJ,et al. HMGB1 Binds to Lipoteichoic Acid and Enhances TNF-alpha and IL-6 Production through HMGB1-Mediated Transfer of Lipoteichoic Acid to CD14 and TLR2 [J]. J Innate Immun,2015,7(4):405-416.
[32] Wang C,Jiang J,Zhang X,et al. Inhibiting HMGB1 Reduces Cerebral Ischemia Reperfusion Injury in Diabetic Mice [J]. Inflammation,2016,39(6):1862-1870.
[33] Kumar P,Yadav AK,Kumar A,et al. Association between Interleukin-6 (G174C and G572C) promoter gene polymorphisms and risk of ischaemic stroke:A meta-analysis [J]. Ann Neurosci,2015,22(2):61-69.
[34] Schroder K,Zhou R,Tschopp J. The NLRP3 inflammasome:a sensor for metabolic danger? [J]. Science,2010, 327(5963):296-300.
[35] Hong P,Li FX,Gu RN,et al. Inhibition of NLRP3 Inflammasome Ameliorates Cerebral Ischemia-Reperfusion Injury in Diabetic Mice [J]. Neural Plast,2018,2018:9163521.
[36] Ward R,Li W,Abdul Y,et al. NLRP3 inflammasome inhibition with MCC950 improves diabetes-mediated cognitive impairment and vasoneuronal remodeling after ischemia [J]. Pharmacol Res,2019,142:237-250.
[37] Soveid M,Dehghani GA,Omrani GR. Long- term efficacy and safety of vanadium in the treatment of type 1 diabetes [J]. Arch Iran Med,2013,16(7):408-411.
[38] Ahmadi-Eslamloo H,Moosavi S,Dehghani GA. Cerebral Ischemia-Reperfusion Injuries in Vanadyl-Treated Diabetic Rats [J]. Iran J Med Sci,2017,42(6):544-552.
[39] 曾滋,张云砚,陈榕,等.Parkin在糖尿病鼠肠缺血再灌注所致肠损伤易损性增加中的作用[J].武汉大学学报:医学版,2018,39(3):356-360.
[40] Kinoshita H,Nakajima Y,Uramoto H. Anomalous Pulmonary Arterial Supply to the Pulmonary Vein of the Right Lung:An Extremely Exceptional Case of Arterial Vein Fistulae [J]. Ann Thorac Surg,2015,100(5):1913. |
|
|
|