Citation: | ZHANG Xi, HUANG Bing, WANG Guipeng. Progress of NLRP3 Inflammasome and Myocardial Ischemia Reperfusion Injury[J]. Medical Journal of Peking Union Medical College Hospital, 2022, 13(2): 296-301. DOI: 10.12290/xhyxzz.2021-0619 |
[1] |
胡盛涛, 高润霖, 刘力生, 等. 《中国心血管病报告2018》概要[J]. 中国循环杂志, 2019, 34: 209-220. DOI: 10.3969/j.issn.1000-3614.2019.03.001
Hu SS, Gao RL, Liu LS, et al. Summary of The Chinese Cardiovascular Disease Report 2018[J]. Zhongguo Xunhuan Zazhi, 2019, 34: 209-220. DOI: 10.3969/j.issn.1000-3614.2019.03.001
|
[2] |
Takahashi J, Yamamoto M, Yasukawa H, et al. Interleukin-22 Directly Activates Myocardial STAT3 (Signal Transducer and Activator of Transcription-3) Signaling Pathway and Prevents Myocardial Ischemia Reperfusion Injury[J]. J Am Heart Assoc, 2020, 9: e014814. DOI: 10.1161/JAHA.119.014814
|
[3] |
Wang Z, Zhang SM, Xiao Y, et al. NLRP3 Inflammasome and Inflammatory Diseases[J]. Oxid Med Cell Longev, 2020, 2020: 4063562.
|
[4] |
Zeng C, Wang R, Tan H. Role of pyroptosis incardiovASCular diseases and its therapeutic implications[J]. Int J Biol Sci, 2019, 15: 1345-1357. DOI: 10.7150/ijbs.33568
|
[5] |
Yang X, Lin G, Han Z, et al. Structural Biology of nod-Like Receptors[J]. Adv Exp Med Biol, 2019, 1172: 119-141.
|
[6] |
Lu A, Magupalli VG, Ruan J, et al. Unified polymerization mechanism for the assembly of ASC-dependent inflamma-somes[J]. Cell, 2014, 156: 1193-1206. DOI: 10.1016/j.cell.2014.02.008
|
[7] |
Zheng DP, Liwinski T, Elinav E. Inflammasome activation and regulation: toward a better understanding of complex mechanisms[J]. Cell Discov, 2020, 6: 36.
|
[8] |
Gong W, Shi Y, Ren J. Research progresses of molecular mechanism of pyroptosis and its related diseases[J]. Immunobiology, 2020, 225: 151884. DOI: 10.1016/j.imbio.2019.11.019
|
[9] |
Hooftman A, Angiari S, Hester S, et al. The Immunomodulatory Metabolite Itaconate Modifies NLRP3 and Inhibits Inflammasome Activation[J]. Cell Metab, 2020, 32: 468-478.e7. DOI: 10.1016/j.cmet.2020.07.016
|
[10] |
Guo Q, Wu Y, Hou Y, et al. Cytokine secretion and pyroptosis of thyroid follicular cells mediated by enhanced NLRP3, NLRP1, NLRC4, and AIM2 inflammasomes are associated with autoimmune thyroiditis[J]. Front Immunol, 2018, 9: 1197. DOI: 10.3389/fimmu.2018.01197
|
[11] |
Yu P, Li YG, Fu WW, et al. Panax quinquefolius L. Saponins Protect Myocardial ischemia Reperfusion No-Reflow Through Inhibiting the Activation of NLRP3 Inflammasome via TLR4/MyD88/Nf-κB Signaling Pathway[J]. Front Pharmacol, 2020, 11: 607813.
|
[12] |
Amin J, Boche D, Rakic S. What do we know about the inflammasome in humans?[J]. Brain Pathol, 2017, 27: 192-204. DOI: 10.1111/bpa.12479
|
[13] |
Lei Q, Yi T, Chen C. NF-kappaB-Gasdermin D axis couples oxidative stress and NACHT, LRR and PYD domainscontaining protein 3 inflammasome-mediatedcardio-myocyte pyroptosis following myocardial infarction[J]. Med Sci Monit, 2018, 24: 6044-6052. DOI: 10.12659/MSM.908529
|
[14] |
Minutoli L, Puzzolo D, Rinaldi M, et al. ROS-Mediated NLRP3 inflammasome activation in brain, heart, kidney, and testis ischemia/reperfusion injury[J]. Oxid Med Cell Longev, 2016, 2016: 2183026.
|
[15] |
Cinteza M. OK-Flow. Sorry-No-Reflow[J]. Maedica (Bucur), 2019, 14: 323-325.
|
[16] |
Dai YX, Wang S, Chang SF, et al. M2 macrophage-derived exosomes carry microRNA-148a to alleviate myocardial ischemia/reperfusion injury via inhibiting TXNIP and the TLR4/NF-κB/NLRP3 inflammasome signaling pathway[J]. J Mol Cell Cardiol, 2020, 142: 65-79. DOI: 10.1016/j.yjmcc.2020.02.007
|
[17] |
Hesse J, Leberling S, Boden E, et al. CD73-derived adenosine and tenASCin-C control cytokine production by epicardium-derived cells formed after myocardial infarction[J]. FASEB J, 2017, 31: 3040-3053. DOI: 10.1096/fj.201601307R
|
[18] |
Deng Y, Han X, Yao Z, et al. PPARalpha Agonist Stimulated Angiogenesis by Improving Endothelial Precursor Cell Function Via a NLRP3 Inflammasome Pathway[J]. Cell Physiol Biochem, 2017, 42: 2255-2266. DOI: 10.1159/000479999
|
[19] |
Westerterp M, Fotakis P, Ouimet M, et al. Cholesterol Efflux Pathways Suppress Inflammasome Activation, NETosis, and Atherogene-sis[J]. Circulation, 2018, 138: 898-912. DOI: 10.1161/CIRCULATIONAHA.117.032636
|
[20] |
Sun WJ, Dong SJ, Lu HQ, et al. Beclin-1 overexpression regulates NLRP3 activation by promoting TNFAIP3 in microvASCular injury following myocardial reperfusion[J]. Cell Signal, 2021, 84: 110008. DOI: 10.1016/j.cellsig.2021.110008
|
[21] |
Zhou T, Xiang DK, Li SN, et al. MicroRNA-495 Amelio-rates Cardiac Microvascular Endothelial Cell Injury and Inflammatory Reaction by Suppressing the NLRP3 Inflamma-some Signaling Pathway[J]. Cell Physiol Biochem, 2018, 49: 798-815. DOI: 10.1159/000493042
|
[22] |
van Hout GP, Bosch L, Ellenbroek GH, et al. The selective NLRP3-inflammasome inhibitor MCC950 reduces infarct size and preserves cardiac function in a pig model of myocardial infarction[J]. Eur Heart J, 2017, 38: 828-836.
|
[23] |
Penna C, Aragno M, Cento AS, et al. Ticagrelor Conditioning Effects Are Not Additive to Cardioprotection Induced by Direct NLRP3 Inflammasome Inhibition: Role of RISK, NLRP3, and Redox Cascades[J]. Oxid Med Cell Longev, 2020, 2020: 9219825.
|
[24] |
Wang L, Peng YF, Song LJ, et al. Colchicine-Containing Nanoparticles Attenuates Acute Myocardial Infarction Injury by Inhibiting Inflammation[J]. Cardiovasc Drugs Ther, 2021. doi: 10.1007/s10557-021-07239-2.
|
[25] |
Opstal TSJ, Fiolet ATL, van Broekhoven A, et al. Colchicine in Patients With Chronic Coronary Disease in Relation to Prior Acute Coronary Syndrome[J]. J Am Coll Cardiol, 2021, 78: 859-866. DOI: 10.1016/j.jacc.2021.06.037
|
[26] |
Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in patients with chronic coronary disease[J]. N Engl J Med, 2020, 383: 1838-1847. DOI: 10.1056/NEJMoa2021372
|
[27] |
Schattner A. Colchicine-new horizons for an ancient drug. Review based on the highest hierarchy of evidence[J]. Eur J Intern Med, 2022, 96: 34-41. DOI: 10.1016/j.ejim.2021.10.002
|
[28] |
Leung YY, Yao Hui LL, Kraus VB. Colchicine--Update on mechanisms of action and therapeutic uses[J]. Semin Arthritis Rheum, 2015, 45: 341-350. DOI: 10.1016/j.semarthrit.2015.06.013
|
[29] |
Su XL, Wang SH, Komal S, et al. The caspase-1 inhibitor VX765 upregulates connexin 43 expression and improves cell-cell communication after myocardial infarction via suppressing the IL-1β/p38 MAPK pathway[J]. Acta Pharmacol Sin, 2022. doi: 10.1038/s41401-021-00845-8.
|
[30] |
Yang XM, Downey JM, Cohen MV, et al. The Highly Selective Caspase-1 Inhibitor VX-765 Provides Additive Protec-tion Against Myocardial Infarction in Rat Hearts When Combined With a Platelet Inhibitor[J]. J Cardiovasc Pharmacol Ther, 2017, 22: 574-578. DOI: 10.1177/1074248417702890
|
[31] |
Do Carmo H, Arjun S, Petrucci O, et al. The Caspase 1 Inhibitor VX-765 Protects the Isolated Rat Heart via the RISK Pathway[J]. Cardiovasc Drugs Ther, 2018, 32: 165-168. DOI: 10.1007/s10557-018-6781-2
|
[32] |
Luo YF, Xiong BJ, Liu HP, et al. Koumine Suppresses IL-1β Secretion and Attenuates Inflammation Associated With Blocking ROS/NF-κB/NLRP3 Axis in Macrophages[J]. Front Pharmacol, 2020, 11: 622074.
|
[33] |
Nazir S, Gadi I, Al-Dabet MM, et al. Cytoprotective activated protein C averts NLRP3 inflammasome-induced ischemia-reperfusion injury via mTORC1 inhibition[J]. Blood, 2017, 130: 2664-2677. DOI: 10.1182/blood-2017-05-782102
|
[34] |
Jun JH, Shim JK, Oh JE, et al. Protective Effect of Ethyl Pyruvate against Myocardial Ischemia Reperfusion Injury through Regulations of ROS-Related NLRP3 Inflammasome Activation[J]. Oxid Med Cell Longev, 2019, 2019: 4264580.
|
[35] |
Lu QY, Ma JQ, Duan YY, et al. Carthamin Yellow Protects the Heart Against Ischemia/Reperfusion Injury With Reduced Reactive Oxygen Species Release and Inflammatory Response[J]. J Cardiovasc Pharmacol, 2019, 74: 228-234. DOI: 10.1097/FJC.0000000000000710
|
[36] |
Chen A, Chen ZW, Xia Y, et al. Liraglutide attenuates NLRP3 inflammasome-dependent pyroptosis via regulating SIRT1/NOX4/ROS pathway in H9c2 cells[J]. Biochem Biophys Res Commun, 2018, 499: 267-272. DOI: 10.1016/j.bbrc.2018.03.142
|
[37] |
Sun Q, Fan J, Billiar TR, et al. Inflammasome and autophagy regulation a two-way street[J]. Mol Med, 2017, 23: 188-195.
|
[38] |
Iyer SS, He Q, Janczy JR, et al. Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation[J]. Immunity, 2013, 39: 311-323. DOI: 10.1016/j.immuni.2013.08.001
|
[39] |
Li J, Zhao CT, Zhu Q, et al. Sweroside Protects Against Myocardial ischemia-Reperfusion Injury by Inhibiting Oxidative Stress and Pyroptosis Partially via Modulation of the Keap1/Nrf2 Axis[J]. Frontcardiovasc Med, 2021, 8: 650368.
|
[40] |
Guo X, Hu S, Liu JJ, et al. Piperine protects against pyroptosis in myocardial ischaemia/reperfusion injury by regulating the mir-383/RP105/AKT signalling pathway[J]. J Cell Mol Med, 2021, 25: 244-258. DOI: 10.1111/jcmm.15953
|
[41] |
Zuo W, Tian R, Chen Q, et al. miR-330-5p inhibits NLRP3 inflammasome mediated myocardial ischaemia-reperfusion injury by targeting TIM3[J]. Cardiovasc Drugs Ther, 2021, 35: 691-705. DOI: 10.1007/s10557-020-07104-8
|
[42] |
Jiang S, Cui H, Wu P, et al. Botany, traditional uses, phytochemistry, pharmacology and toxicology of Ilex pubescens Hook et Arn[J]. J Ethnopharmacol, 2019, 245: 112147. DOI: 10.1016/j.jep.2019.112147
|
[43] |
Cheng YY, Cheng LK, Gao X, et al. Covalent modification of Keap1 at Cys77 and Cys434 by pubescenoside a sup-presses oxidative stress-induced NLRP3 inflammasome activation in Myocardial ischemia-reperfusion injury[J]. Theranostics, 2021, 11: 861-877. DOI: 10.7150/thno.48436
|
[44] |
Xiao Y, Oumarou DB, Wang S, et al. Malva Sylvestris Circular RNA Involved in the Protective Effect of Malva Sylvestris L. on Myocardial ischemic/Re-Perfused Injury[J]. Front Pharmacol, 2020, 11: 520486. DOI: 10.3389/fphar.2020.520486
|
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