References: Heusch G, Kleinbongard P, Skyschally A, Levkau B, Schulz R, Erbel R. The coronary circulation in cardioprotection: more than just one confounder. Cardiovasc Res. 2012;94(2):237-245. https://doi.org/10.1093/cvr/cvr271.
Gerczuk PZ, Kloner RA. Protecting the heart from ischemia: an update on ischemic and pharmacologic conditioning. Hosp Pract (1995). 2011;39(3):35-43. https://doi.org/10.3810/hp.2011.08.577.
Bousselmi R, Lebbi MA, Ferjani M. Myocardial ischemic conditioning: physiological aspects and clinical applications in cardiac surgery. J Saudi Heart Assoc. 2014;26(2):93-100. https://doi.org/10.1016/j.jsha.2013.11.001.
Zhao Z-Q, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003;285(2):H579-H588. https://doi.org/10.1152/ajpheart.01064.2002.
Argaud L, Gateau-Roesch O, Augeul L, et al. Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts. Am J Physiol Heart Circ Physiol. 2008;294(1):H386-H391. https://doi.org/10.1152/ajpheart.01035.2007.
Luo W, Li B, Lin G, Huang R. Postconditioning in cardiac surgery for tetralogy of Fallot. J Thorac Cardiovasc Surg. 2007;133(5):1373-1374. https://doi.org/10.1016/j.jtcvs.2007.01.028.
Badalzadeh R, Baradaran B, Alihemmati A, Yousefi B, Abbaszadeh A. Troxerutin preconditioning and ischemic postconditioning modulate inflammatory response after myocardial ischemia/reperfusion injury in rat model. Inflammation. 2017;40(1):136-143. https://doi.org/10.1007/s10753-016-0462-8.
Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc Res. 1999;43(4):860-878. https://doi.org/10.1016/s0008-6363(99)00187-x.
Francis A, Baynosa R. Ischaemia-reperfusion injury and hyperbaric oxygen pathways: a review of cellular mechanisms. Diving Hyperb Med. 2017;47(2):110-117. https://doi.org/10.28920/dhm47.2.110-117.
Wu M-Y, Yiang G-T, Liao W-T, et al. Current mechanistic concepts in ischemia and reperfusion injury. Cell Physiol Biochem. 2018;46(4):1650-1667. https://doi.org/10.1159/000489241.
Hu C, Dandapat A, Chen J, et al. LOX-1 deletion alters signals of myocardial remodeling immediately after ischemia-reperfusion. Cardiovasc Res. 2007;76(2):292-302. https://doi.org/10.1016/j.cardiores.2007.07.003.
Marzilli M, Morrone D, Guarini G. Postconditioning. Heart Metab. 2012;54:20-24.
Walker MJA, Curtis MJ, Hearse DJ, et al. The lambeth conventions: guidelines for the study of arrhythmias in ischaemia infarction, and reperfusion. Cardiovasc Res. 1988;22(7):447-455. https://doi.org/10.1093/cvr/22.7.447.
Kaneko T, Hayashida M, Saito Y, Hikawa Y, Yasuda K. Myocardial ischemia score as a preoperative screening method for intraoperative myocardial ischemia. Masui. 2000;49(2):145-149.
Sahna E, Acet A, Ozer MK, Olmez E. Myocardial ischemia-reperfusion in rats: reduction of infarct size by either supplemental physiological or pharmacological doses of melatonin. J Pineal Res. 2002;33(4):234-238.
Ozyıldırım S, Baltaci AK, Sahna E, Mogulkoc R. Effects of chronic and acute zinc supplementation on myocardial ischemia-reperfusion injury in rats. Biol Trace Elem Res. 2017;178(1):64-70. https://doi.org/10.1007/s12011-016-0903-0.
Wei C, Li H, Han L, Zhang L, Yang X. Activation of autophagy in ischemic postconditioning contributes to cardioprotective effects against ischemia/reperfusion injury in rat hearts. J Cardiovasc Pharmacol. 2013;61(5):416-422. https://doi.org/10.1097/FJC.0b013e318287d501.
Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-delta delta C(T)) method. Methods. 2001;25(4):402-408. https://doi.org/10.1006/meth.2001.1262.
Dan Dunn J, Alvarez LA, Zhang X, Soldati T. Reactive oxygen species and mitochondria: a nexus of cellular homeostasis. Redox Biol. 2015;6:472-485. https://doi.org/10.1016/j.redox.2015.09.005.
Bedard K, Krause K-H. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol Rev. 2007;87(1):245-313. https://doi.org/10.1152/physrev.00044.2005.
Matsushima S, Tsutsui H, Sadoshima J. Physiological and pathological functions of NADPH oxidases during myocardial ischemia-reperfusion. Trends Cardiovasc Med. 2014;24(5):202-205. https://doi.org/10.1016/j.tcm.2014.03.003.
Huang J, Canadien V, Lam GY, et al. Activation of antibacterial autophagy by NADPH oxidases. Proc Natl Acad Sci U S A. 2009;106(15):6226-6231. https://doi.org/10.1073/pnas.0811045106.
Braunersreuther V, Montecucco F, Ashri M, et al. Role of NADPH oxidase isoforms NOX1, NOX2 and NOX4 in myocardial ischemia/reperfusion injury. J Mol Cell Cardiol. 2013;64:99-107. https://doi.org/10.1016/j.yjmcc.2013.09.007.
He F, Liu H, Guo J, et al. Inhibition of microRNA-124 reduces cardiomyocyte apoptosis following myocardial infarction via targeting STAT3. Cell Physiol Biochem. 2018;51(1):186-200. https://doi.org/10.1159/000495173.
Yu B, Meng F, Yang Y, Liu D, Shi K. NOX2 antisense attenuates hypoxia-induced oxidative stress and apoptosis in cardiomyocyte. Int J Med Sci. 2016;13(8):646-652. https://doi.org/10.7150/ijms.15177.
Bell RM, Cave AC, Johar S, Hearse DJ, Shah AM, Shattock MJ. Pivotal role of NOX-2-containing NADPH oxidase in early ischemic preconditioning. FASEB J. 2005;19(14):2037-2039. https://doi.org/10.1096/fj.04-2774fje.
Yao W, Han X, Zhang Y, et al. Intravenous anesthetic protects hepatocyte from reactive oxygen species-induced cellular apoptosis during liver transplantation in vivo. Oxid Med Cell Longev. 2018;2018:4780615. https://doi.org/10.1155/2018/4780615.
Small EM, Olson EN. Pervasive roles of microRNAs in cardiovascular biology. Nature. 2011;469(7330):336-342. https://doi.org/10.1038/nature09783.
Ren X-P, Wu J, Wang X, et al. MicroRNA-320 is involved in the regulation of cardiac ischemia/reperfusion injury by targeting heat-shock protein 20. Circulation. 2009;119(17):2357-2366. https://doi.org/10.1161/CIRCULATIONAHA.108.814145.
Varga ZV, Zvara Á, Faragó N, et al. MicroRNAs associated with ischemia-reperfusion injury and cardioprotection by ischemic pre- and postconditioning: protectomiRs. Am Jo Physiol Heart Circ Physiol. 2014;307(2):H216-H227. https://doi.org/10.1152/ajpheart.00812.2013.
Liu Z, Tuo Y-H, Chen J-W, et al. NADPH oxidase inhibitor regulates microRNAs with improved outcome after mechanical reperfusion. J Neurointerv Surg. 2017;9(7):702-706. https://doi.org/10.1136/neurintsurg-2016-012463.
Sengupta A, Molkentin JD, Yutzey KE. FoxO transcription factors promote autophagy in cardiomyocytes. J Biol Chem. 2009;284(41):28319-28331. https://doi.org/10.1074/jbc.M109.024406.
Wang Q, Guo W, Hao B, et al. Mechanistic study of TRPM2-Ca(2+)-CAMK2-BECN1 signaling in oxidative stress-induced autophagy inhibition. Autophagy. 2016;12(8):1340-1354. https://doi.org/10.1080/15548627.2016.1187365.
Zhang D, Zhang W, Li D, Fu M, Chen R, Zhan Q. GADD45A inhibits autophagy by regulating the interaction between BECN1 and PIK3C3. Autophagy. 2015;11(12):2247-2258. https://doi.org/10.1080/15548627.2015.1112484.
Mei Y, Glover K, Su M, Sinha SC. Conformational flexibility of BECN1: essential to its key role in autophagy and beyond. Protein Sci. 2016;25(10):1767-1785. https://doi.org/10.1002/pro.2984.
Zhu H, He L. Beclin 1 biology and its role in heart disease. Curr Cardiol Rev. 2015;11(3):229-237.
Pal R, Bajaj L, Sharma J, et al. NADPH oxidase promotes Parkinsonian phenotypes by impairing autophagic flux in an mTORC1-independent fashion in a cellular model of Parkinson's disease. Sci Rep. 2016;6:22866. https://doi.org/10.1038/srep22866.
Liu G, Yuan Y, Long M, et al. Beclin-1-mediated autophagy protects against cadmium-activated apoptosis via the Fas/FasL pathway in primary rat proximal tubular cell culture. Sci Rep. 2017;7(1):977. https://doi.org/10.1038/s41598-017-00997-w.
Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol. 2007;35(4):495-516. https://doi.org/10.1080/01926230701320337.
Woo SH, Park IC, Park MJ, et al. Arsenic trioxide sensitizes CD95/Fas-induced apoptosis through ROS-mediated upregulation of CD95/Fas by NF-κB activation. Int J Cancer. 2004;112(4):596-606. https://doi.org/10.1002/ijc.20433.
Ham O, Lee S-Y, Song B-W, et al. Modulation of Fas-Fas ligand interaction rehabilitates hypoxia-induced apoptosis of mesenchymal stem cells in ischemic myocardium niche. Cell Transplant. 2015;24(7):1329-1341. https://doi.org/10.3727/096368914X681748.
He S-F, Zhu H-J, Han Z-Y, et al. MicroRNA-133b-5p is involved in cardioprotection of morphine preconditioning in rat cardiomyocytes by targeting Fas. Can J Cardiol. 2016;32(8):996-1007. https://doi.org/10.1016/j.cjca.2015.10.019.
Teplyakov AT, Berezikova EN, Shilov SN, et al. Role of soluble Fas ligand in myocardial remodeling, severity and outcomes of chronic heart failure. Ter Arkh. 2016;88(9):10-16. https://doi.org/10.17116/terarkh201688910-16.
Szymanowski A, Li W, Lundberg A, et al. Soluble Fas ligand is associated with natural killer cell dynamics in coronary artery disease. Atherosclerosis. 2014;233(2):616-622. https://doi.org/10.1016/j.atherosclerosis.2014.01.030.
Zhang L, Zhang L, Li Y, Chen M, Zhang H, Gao M. Effects of high dose glucose-insulin-potassium infusion on myocardial injury and serum sFas/sFasL concentration in acute myocardial infarction. Zhonghua Nei Ke Za Zhi. 2005;44(7):499-502.
Tong T, Ji J, Jin S, et al. Gadd45a expression induces bim dissociation from the cytoskeleton and translocation to mitochondria. Mol Cell Biol. 2005;25(11):4488-4500. https://doi.org/10.1128/MCB.25.11.4488-4500.2005.
Wang N, Yang C, Xie F, et al. Gadd45α: a novel diabetes-associated gene potentially linking diabetic cardiomyopathy and baroreflex dysfunction. PLoS One. 2012;7(12):e49077. https://doi.org/10.1371/journal.pone.0049077.
Yang G, Zhu Y, Dong X, Duan Z, Niu X, Wei J. TLR2-ICAM1-Gadd45α axis mediates the epigenetic effect of selenium on DNA methylation and gene expression in Keshan disease. Biol Trace Elem Res. 2014;159(1-3):69-80. https://doi.org/10.1007/s12011-014-9985-8.
Zhu H-J, Han Z-Y, He S-F, et al. Specific MicroRNAs comparisons in hypoxia and morphine preconditioning against hypoxia-reoxgenation injury with and without heart failure. Life Sci. 2017;170:82-92. https://doi.org/10.1016/j.lfs.2016.11.028.
He Y, Liu J-N, Zhang J-J, Fan W. Involvement of microRNA-181a and Bim in a rat model of retinal ischemia-reperfusion injury. Int J Ophthalmol. 2016;9(1):33-40. https://doi.org/10.18240/ijo.2016.01.06.
Ramasamy S, Velmurugan G, Shanmugha Rajan K, Ramprasath T, Kalpana K. MiRNAs with apoptosis regulating potential are differentially expressed in chronic exercise-induced physiologically hypertrophied hearts. PLoS One. 2015;10(3):e0121401. https://doi.org/10.1371/journal.pone.0121401.
Shao B, Liao L, Yu Y, et al. Estrogen preserves Fas ligand levels by inhibiting microRNA-181a in bone marrow-derived mesenchymal stem cells to maintain bone remodeling balance. FASEB J. 2015;29(9):3935-3944. https://doi.org/10.1096/fj.15-272823.
Zou C, Chen J, Chen K, et al. Functional analysis of miR-181a and Fas involved in hepatitis B virus-related hepatocellular carcinoma pathogenesis. Exp Cell Res. 2015;331(2):352-361. https://doi.org/10.1016/j.yexcr.2014.11.007.
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