参考文献/References:
[1] Hausenloy DJ,Chilian W,Crea F,et al. The coronary circulation in acute myocardial ischaemia/reperfusion injury:a target for cardioprotection[J]. Cardiovasc Res,2019,115(7):1143-1155.
[2] Kalogeris T,Baines CP,Krenz M,et al. Ischemia/Reperfusion[J]. Compr Physiol,2016,7(1):113-170.
[3] Davidson SM,Ferdinandy P,Andreadou I,et al. Multitarget strategies to reduce myocardial ischemia/reperfusion injury: JACC review topic of the week[J]. J Am Coll Cardiol ,2019,73(1):89-99.
[4] Zhong W,Benissan-Messan DZ,Ma J,et al. Cardiac effects and clinical applications of MG53[J]. Cell Biosci,2021,11(1):115.
[5] Li Y,Meng Q,Wang L,et al.TRIM27 protects against cardiac ischemia-reperfusion injury by suppression of apoptosis and inflammation via negatively regulating p53[J]. Biochem Biophys Res Commun,2021,557:127-134.
[6] Esposito D,Koliopoulos MG,Rittinger K.Structural determinants of TRIM protein function[J]. Biochem Soc Trans,2017,45(1):183-191.
[7] Bell JL,Malyukova A,Holien JK,et al.TRIM16 acts as an E3 ubiquitin ligase and can heterodimerize with other TRIM family members[J]. PLoS One,2012,7(5):e37470.
[8] Sanchez JG,Okreglicka K,Chandrasekaran V,et al. The tripartite motif coiled-coil is an elongated antiparallel hairpin dimer[J]. Proc Natl Acad Sci USA,2014,111(7):2494-2499.
[9] Hatakeyama S. TRIM proteins and cancer[J]. Nat Rev Cancer,2011,11(11):792-804.
[10] Sparrer K,Gack MU.TRIM proteins:new players in virus-induced autophagy[J]. PLoS Pathog,2018,14(2):e1006787.
[11] Alloush J,Weisleder N. TRIM proteins in therapeutic membrane repair of muscular dystrophy[J]. JAMA Neurol,2013,70(7):928-931.
[12] Kudryashova E,Kudryashov D,Kramerova I,et al. Trim32 is a ubiquitin ligase mutated in limb girdle muscular dystrophy type 2H that binds to skeletal muscle myosin and ubiquitinates actin[J]. J Mol Biol,2005,354(2):413-424.
[13] Borlepawar A,Rangrez AY,Bernt A,et al. TRIM24 protein promotes and TRIM32 protein inhibits cardiomyocyte hypertrophy via regulation of dysbindin protein levels[J]. J Biol Chem,2017,292(24):10180-10196.
[14] Lorenzana-Carrillo MA,Gopal K,Byrne NJ,et al. TRIM35-mediated degradation of nuclear PKM2 destabilizes GATA4/6 and induces P53 in cardiomyocytes to promote heart failure[J]. Sci Transl Med,2022,14(669):m3565.
[15] Jennings RB.Historical perspective on the pathology of myocardial ischemia/reperfusion injury[J]. Circ Res,2013,113(4):428-438.
[16] Hernandez-Deviez DJ,Howes MT,Laval SH,et al. Caveolin regulates endocytosis of the muscle repair protein,dysferlin[J]. J Biol Chem,2008,283(10):6476-6488.
[17] Cai C,Masumiya H,Weisleder N,et al. MG53 nucleates assembly of cell membrane repair machinery[J]. Nat Cell Biol,2009,11(1):56-64.
[18] Wang X,Xie W,Zhang Y,et al. Cardioprotection of ischemia/reperfusion injury by cholesterol-dependent MG53-mediated membrane repair[J]. Circ Res,2010,107(1):76-83.
[19] Cai C,Lin P,Zhu H,et al. Zinc binding to MG53 protein facilitates repair of injury to cell membranes[J]. J Biol Chem,2015,290(22):13830-13839.
[20] Garcia N,Zazueta C,Aguilera-Aguirre L. Oxidative stress and inflammation in cardiovascular disease[J]. Oxid Med Cell Longev,2017,2017:5853238.
[21] Dang X,Qin Y,Gu C,et al. Knockdown of tripartite motif 8 protects H9C2 cells against hypoxia/reoxygenation-induced injury through the activation of PI3K/Akt signaling pathway[J]. Cell Transplant,2020,29:2138941951.
[22] Lu B,Li J,Gui M,et al. Salvianolic acid B inhibits myocardial I/R-induced ROS generation and cell apoptosis by regulating the TRIM8/GPX1 pathway[J]. Pharm Biol,2022,60(1):1458-1468.
[23] Jena KK,Kolapalli SP,Mehto S,et al. TRIM16 controls turnover of protein aggregates by modulating NRF2,ubiquitin system,and autophagy:implication for tumorigenesis[J]. Mol Cell Oncol,2018,5(6):e1532251.
[24] Cui Q,Yan L.Tripartite motif-containing protein 16 protects against myocardial ischemia/reperfusion injury by affecting the Keap1/Nrf2 axis[J]. Cell Tissue Res,2021,386(2):349-363.
[25] Gumpper-Fedus K,Park KH,Ma H,et al. MG53 preserves mitochondrial integrity of cardiomyocytes during ischemia reperfusion-induced oxidative stress[J].Redox Biol,2022,54:102357.
[26] Zhang W,Zhang Y,Zhang H,et al. USP49 inhibits ischemia-reperfusion-induced cell viability suppression and apoptosis in human AC16 cardiomyocytes through DUSP1-JNK1/2 signaling[J]. J Cell Physiol,2019,234(5):6529-6538.
[27] He F,Wu Z,Wang Y,et al. Downregulation of tripartite motif protein 11 attenuates cardiomyocyte apoptosis after ischemia/reperfusion injury via DUSP1-JNK1/2[J]. Cell Biol Int,2022,46(1):148-157.
[28] Zeng G,Lian C,Yang P,et al. E3-ubiquitin ligase TRIM6 aggravates myocardial ischemia/reperfusion injury via promoting STAT1-dependent cardiomyocyte apoptosis[J]. Aging (Albany NY),2019,11(11):3536-3550.
[29] Dhuriya YK,Sharma D. Necroptosis:a regulated inflammatory mode of cell death[J]. J Neuroinflammation,2018,15(1):199.
[30] Wang Q,Park KH,Geng B,et al. MG53 inhibits necroptosis through ubiquitination-dependent RIPK1 degradation for cardiac protection following ischemia/reperfusion injury[J]. Front Cardiovasc Med,2022,9:868632.
[31] Algoet M,Janssens S,Himmelreich U,et al. Myocardial ischemia-reperfusion injury and the influence of inflammation[J]. Trends Cardiovasc Med,2022,S1050-1738(22):00029-9.
[32] Lu Z,Deng M,Ma G,et al. TRIM38 protects H9c2 cells from hypoxia/reoxygenation injury via the TRAF6/TAK1/NF-κB signalling pathway[J]. Peer J,2022,10:e13815.
[33] Ball DP,Taabazuing CY,Griswold AR,et al. Caspase-1 interdomain linker cleavage is required for pyroptosis[J]. Life Sci Alliance,2020,3(3): e202000664.
[34] Shi M,Su F,Dong Z,et al. TRIM16 exerts protective function on myocardial ischemia/reperfusion injury through reducing pyroptosis and inflammation via NLRP3 signaling[J]. Biochem Biophys Res Commun,2022,632:122-128.
[35] Murry CE,Jennings RB,Reimer KA. Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium[J]. Circulation,1986,74(5):1124-1136.
[36] Heusch G. Molecular basis of cardioprotection:signal transduction in ischemic pre-,post-, and remote conditioning[J]. Circ Res ,2015,116(4):674-699.
[37] Cao CM,Zhang Y,Weisleder N,et al. MG53 constitutes a primary determinant of cardiac ischemic preconditioning[J]. Circulation,2010,121(23):2565-2574.
[38] Shan D,Guo S,Wu HK,et al. Cardiac ischemic preconditioning promotes MG53 secretion through H2O2-activated protein kinase C-δ signaling[J]. Circulation,2020,142(11):1077-1091.
[39] Heusch G. Myocardial ischaemia-reperfusion injury and cardioprotection in perspective[J]. Nat Rev Cardiol,2020,17(12):773-789.
[40] Zhang Y,Lv F,Jin L,et al. MG53 participates in ischaemic postconditioning through the RISK signalling pathway[J]. Cardiovasc Res,2011,91(1):108-115.
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