• ISSN 1674-8301
  • CN 32-1810/R
Turn off MathJax
Article Contents
Natalia V. Naryzhnaya, Leonid N. Maslov, Sergey V. Popov, Alexandr V. Mukhomezyanov, Vyacheslav V. Ryabov, Boris K. Kurbatov, Alexandra E. Gombozhapova, Nirmal Singh, Feng Fu, Jian-Ming Pei, Sergey V. Logvinov. Pyroptosis is a drug target for prevention of adverse cardiac remodeling: The crosstalk between pyroptosis, apoptosis, and autophagy[J]. The Journal of Biomedical Research. doi: 10.7555/JBR.36.20220123
Citation: Natalia V. Naryzhnaya, Leonid N. Maslov, Sergey V. Popov, Alexandr V. Mukhomezyanov, Vyacheslav V. Ryabov, Boris K. Kurbatov, Alexandra E. Gombozhapova, Nirmal Singh, Feng Fu, Jian-Ming Pei, Sergey V. Logvinov. Pyroptosis is a drug target for prevention of adverse cardiac remodeling: The crosstalk between pyroptosis, apoptosis, and autophagy[J]. The Journal of Biomedical Research. doi: 10.7555/JBR.36.20220123

Pyroptosis is a drug target for prevention of adverse cardiac remodeling: The crosstalk between pyroptosis, apoptosis, and autophagy

doi: 10.7555/JBR.36.20220123
More Information
  • Corresponding author: Leonid N. Maslov, Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Kyevskaya 111A, 634012 Tomsk, Russia. E-mail: maslov@cardio-tomsk.ru
  • Received: 2022-05-22
  • Revised: 2022-06-23
  • Accepted: 2022-07-06
  • Published: 2022-08-10
  • Acute myocardial infarction (AMI) is one of the main reasons of disease-related death. The introduction of percutaneous coronary intervention to clinical practice dramatically decreased the mortality rate in AMI. Adverse cardiac remodeling is a serious problem in cardiology. An increase in the effectiveness of AMI treatment and prevention of adverse cardiac remodeling is difficult to achieve without understanding the mechanism(s) of reperfusion cardiac injury and cardiac remodeling. Inhibition of pyroptosis prevents the development of postinfarction and pressure overload-induced cardiac remodeling, mitigated cardiomyopathy induced by diabetes and metabolic syndrome. Therefore, it is reasonable to hypothesize that the pyroptosis inhibitors may find a role in clinical practice for treatment of AMI and prevention of cardiac remodeling, diabetes and metabolic syndrome-triggered cardiomyopathy. It was demonstrated that pyroptosis interacts closely with apoptosis and autophagy. Pyroptosis could be inhibited by nucleotide-binding oligomerization domain-like receptor with a pyrin domain 3 inhibitors, caspase-1 inhibitors, microRNA, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and traditional Chinese herbal medicines.


  • CLC number: R542.2,, Document code: A
    The authors reported no conflict of interests.
  • loading
  • [1]
    Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics-2015 update: a report from the American Heart Association[J]. Circulation, 2015, 131(4): e29–e322. doi: 10.1161/CIR.0000000000000152
    Benjamin EJ, Virani SS, Callaway CW, et al. Heart disease and stroke statistics-2018 update: a report from the American Heart Association[J]. Circulation, 2018, 137(12): e67–e492. doi: 10.1161/CIR.0000000000000558
    De Geest B, Mishra M. Role of high-density lipoproteins in cardioprotection and in reverse remodeling: therapeutic implications[J]. Biochim Biophys Acta Mol Cell Biol Lipids, 2021, 1866(11): 159022. doi: 10.1016/j.bbalip.2021.159022
    D'Elia N, D'hooge J, Marwick TH. Association between myocardial mechanics and ischemic LV remodeling[J]. JACC Cardiovasc Imaging, 2015, 8(12): 1430–1443. doi: 10.1016/j.jcmg.2015.10.005
    van der Bijl P, Abou R, Goedemans L, et al. Left ventricular post-infarct remodeling: implications for systolic function improvement and outcomes in the modern Era[J]. JACC Heart Fail, 2020, 8(2): 131–140. doi: 10.1016/j.jchf.2019.08.014
    Yang C, Shen Y, Lu L, et al. Insulin resistance and dysglycemia are associated with left ventricular remodeling after myocardial infarction in non-diabetic patients[J]. Cardiovasc Diabetol, 2019, 18(1): 100. doi: 10.1186/s12933-019-0904-3
    Ryabov V, Gombozhapova A, Rogovskaya Y, et al. Cardiac CD68+ and stabilin-1+ macrophages in wound healing following myocardial infarction: from experiment to clinic[J]. Immunobiology, 2018, 223(4–5): 413–421,doi: 10.1016/j.imbio.2017.11.006.
    Weil BR, Neelamegham S. Selectins and immune cells in acute myocardial infarction and post-infarction ventricular remodeling: pathophysiology and novel treatments[J]. Front Immunol, 2019, 10: 300. doi: 10.3389/fimmu.2019.00300
    Toldo S, Mezzaroma E, van Tassell BW, et al. Interleukin-1β blockade improves cardiac remodelling after myocardial infarction without interrupting the inflammasome in the mouse[J]. Exp Physiol, 2013, 98(3): 734–745. doi: 10.1113/expphysiol.2012.069831
    Popov SV, Maslov LN, Naryzhnaya NV, et al. The role of pyroptosis in ischemic and reperfusion injury of the heart[J]. J Cardiovasc Pharmacol Ther, 2021, 26(6): 562–574. doi: 10.1177/10742484211027405
    Swanson KV, Deng M, Ting JPY. The NLRP3 inflammasome: molecular activation and regulation to therapeutics[J]. Nat Rev Immunol, 2019, 19(8): 477–489. doi: 10.1038/s41577-019-0165-0
    Martinon F, Burns K, Tschopp J. A molecular platform triggering activation of inflammatory caspases and processing of proIL-β[J]. Mol Cell, 2002, 10(2): 417–426. doi: 10.1016/s1097-2765(02)00599-3
    Poznyak AV, Melnichenko AA, Wetzker R, et al. NLPR3 inflammasomes and their significance for atherosclerosis[J]. Biomedicines, 2020, 8(7): 205. doi: 10.3390/biomedicines8070205
    Sebastian-Valverde M, Pasinetti GM. The NLRP3 inflammasome as a critical actor in the inflammaging process[J]. Cells, 2020, 9(6): 1552. doi: 10.3390/cells9061552
    Silvis MJM, Demkes EJ, Fiolet ATL, et al. Immunomodulation of the NLRP3 inflammasome in atherosclerosis, coronary artery disease, and acute myocardial infarction[J]. J Cardiovasc Trans Res, 2021, 14(1): 23–34. doi: 10.1007/s12265-020-10049-w
    Wang S, Zhu H, Li R, et al. DNA-PKcs interacts with and phosphorylates Fis1 to induce mitochondrial fragmentation in tubular cells during acute kidney injury[J]. Sci Signal, 2022, 15(725): eabh1121. doi: 10.1126/scisignal.abh1121
    He W, Wan H, Hu L, et al. Gasdermin D is an executor of pyroptosis and required for interleukin-1β secretion[J]. Cell Res, 2015, 25(12): 1285–1298. doi: 10.1038/cr.2015.139
    Shi J, Zhao Y, Wang K, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J]. Nature, 2015, 526(7575): 660–665. doi: 10.1038/nature15514
    Wang Q, Wu J, Zeng Y, et al. Pyroptosis: a pro-inflammatory type of cell death in cardiovascular disease[J]. Clin Chim Acta, 2020, 510: 62–72. doi: 10.1016/j.cca.2020.06.044
    Mezzaroma E, Toldo S, Farkas D, et al. The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse[J]. Proc Natl Acad Sci USA, 2011, 108(49): 19725–19730. doi: 10.1073/pnas.1108586108
    Liu A, Gao X, Zhang Q, et al. Cathepsin B inhibition attenuates cardiac dysfunction and remodeling following myocardial infarction by inhibiting the NLRP3 pathway[J]. Mol Med Rep, 2013, 8(2): 361–366. doi: 10.3892/mmr.2013.1507
    Liu W, Zhang X, Zhao M, et al. Activation in M1 but not M2 macrophages contributes to cardiac remodeling after myocardial infarction in rats: a critical role of the calcium sensing receptor/NRLP3 inflammasome[J]. Cell Physiol Biochem, 2015, 35(6): 2483–2500. doi: 10.1159/000374048
    Sano S, Oshima K, Wang Y, et al. Tet2-mediated clonal hematopoiesis accelerates heart failure through a mechanism involving the IL-1β/NLRP3 inflammasome[J]. J Am Coll Cardiol, 2018, 71(8): 875–886. doi: 10.1016/j.jacc.2017.12.037
    Gao R, Shi H, Chang S, et al. The selective NLRP3-inflammasome inhibitor MCC950 reduces myocardial fibrosis and improves cardiac remodeling in a mouse model of myocardial infarction[J]. Int Immunopharmacol, 2019, 74: 105575. doi: 10.1016/j.intimp.2019.04.022
    Li X, Bian Y, Pang P, et al. Inhibition of Dectin-1 in mice ameliorates cardiac remodeling by suppressing NF-κB/NLRP3 signaling after myocardial infarction[J]. Int Immunopharmacol, 2020, 80: 106116. doi: 10.1016/j.intimp.2019.106116
    Gao R, Li X, Xiang H, et al. The covalent NLRP3-inflammasome inhibitor Oridonin relieves myocardial infarction induced myocardial fibrosis and cardiac remodeling in mice[J]. Int Immunopharmacol, 2021, 90: 107133. doi: 10.1016/j.intimp.2020.107133
    Wei Z, Fei Y, Wang Q, et al. Loss of Camk2n1 aggravates cardiac remodeling and malignant ventricular arrhythmia after myocardial infarction in mice via NLRP3 inflammasome activation[J]. Free Radic Biol Med, 2021, 167: 243–257. doi: 10.1016/j.freeradbiomed.2021.03.014
    Aliaga J, Bonaventura A, Mezzaroma E, et al. Preservation of contractile reserve and diastolic function by inhibiting the NLRP3 inflammasome with OLT1177® (Dapansutrile) in a mouse model of severe ischemic cardiomyopathy due to non-reperfused anterior wall myocardial infarction[J]. Molecules, 2021, 26(12): 3534. doi: 10.3390/molecules26123534
    Zhang X, Zhao D, Feng J, et al. LuQi Formula regulates NLRP3 inflammasome to relieve myocardial-infarction-induced cardiac remodeling in mice[J]. Evid Based Complement Alternat Med, 2021, 2021: 5518083. doi: 10.1155/2021/5518083
    Shen J, Fan Z, Sun G, et al. Sacubitril/valsartan (LCZ696) reduces myocardial injury following myocardial infarction by inhibiting NLRP3-induced pyroptosis via the TAK1/JNK signaling pathway[J]. Mol Med Rep, 2021, 24(3): 676. doi: 10.3892/mmr.2021.12315
    Wei Q, Liu H, Liu M, et al. Ramipril attenuates left ventricular remodeling by regulating the expression of activin A-follistatin in a rat model of heart failure[J]. Sci Rep, 2016, 6: 33677. doi: 10.1038/srep33677
    von Lueder TG, Wang BH, Kompa AR, et al. Angiotensin receptor neprilysin inhibitor LCZ696 attenuates cardiac remodeling and dysfunction after myocardial infarction by reducing cardiac fibrosis and hypertrophy[J]. Circ Heart Fail, 2015, 8(1): 71–78. doi: 10.1161/CIRCHEARTFAILURE.114.001785
    Kim HS, No CW, Goo SH, et al. An angiotensin receptor blocker prevents arrhythmogenic left atrial remodeling in a rat post myocardial infarction induced heart failure model[J]. J Korean Med Sci, 2013, 28(5): 700–708. doi: 10.3346/jkms.2013.28.5.700
    Nie C, Zou R, Pan S, et al. Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats[J]. J Cell Mol Med, 2021, 25(18): 8997–9010. doi: 10.1111/jcmm.16863
    Luo B, Li B, Wang W, et al. NLRP3 gene silencing ameliorates diabetic cardiomyopathy in a type 2 diabetes rat model[J]. PLoS One, 2014, 9(8): e104771. doi: 10.1371/journal.pone.0104771
    Birnbaum Y, Tran D, Bajaj M, et al. DPP-4 inhibition by linagliptin prevents cardiac dysfunction and inflammation by targeting the Nlrp3/ASC inflammasome[J]. Basic Res Cardiol, 2019, 114(5): 35. doi: 10.1007/s00395-019-0743-0
    Chen H, Tran D, Yang HC, et al. Dapagliflozin and ticagrelor have additive effects on the attenuation of the activation of the NLRP3 inflammasome and the progression of diabetic cardiomyopathy: an AMPK-mTOR interplay[J]. Cardiovasc Drugs Ther, 2020, 34(4): 443–461. doi: 10.1007/s10557-020-06978-y
    Wu X, Liu Y, Tu D, et al. Role of NLRP3-inflammasome/caspase-1/galectin-3 pathway on atrial remodeling in diabetic rabbits[J]. J Cardiovasc Trans Res, 2020, 13(5): 731–740. doi: 10.1007/s12265-020-09965-8
    Elmadbouh I, Singla DK. BMP-7 attenuates inflammation-induced pyroptosis and improves cardiac repair in diabetic cardiomyopathy[J]. Cells, 2021, 10(10): 2640. doi: 10.3390/cells10102640
    Mao S, Chen P, Pan W, et al. Exacerbated post-infarct pathological myocardial remodelling in diabetes is associated with impaired autophagy and aggravated NLRP3 inflammasome activation[J]. ESC Heart Fail, 2022, 9(1): 303–317. doi: 10.1002/ehf2.13754
    Kar S, Shahshahan HR, Hackfort BT, et al. Exercise training promotes cardiac hydrogen sulfide biosynthesis and mitigates pyroptosis to prevent high-fat diet-induced diabetic cardiomyopathy[J]. Antioxidants (Basel), 2019, 8(12): 638. doi: 10.3390/antiox8120638
    Logvinov SV, Naryzhnaya NV, Kurbatov BK, et al. High carbohydrate high fat diet causes arterial hypertension and histological changes in the aortic wall in aged rats: the involvement of connective tissue growth factors and fibronectin[J]. Exp Gerontol, 2021, 154: 111543. doi: 10.1016/j.exger.2021.111543
    Zhao P, Zhou W, Zhang Y, et al. Aminooxyacetic acid attenuates post-infarct cardiac dysfunction by balancing macrophage polarization through modulating macrophage metabolism in mice[J]. J Cell Mol Med, 2020, 24(4): 2593–2609. doi: 10.1111/jcmm.14972
    Sokolova M, Sjaastad I, Louwe MC, et al. NLRP3 inflammasome promotes myocardial remodeling during diet-induced obesity[J]. Front Immunol, 2019, 10: 1621. doi: 10.3389/fimmu.2019.01621
    Chen X, Li H, Wang K, et al. Aerobic exercise ameliorates myocardial inflammation, fibrosis and apoptosis in high-fat-diet rats by inhibiting P2X7 purinergic receptors[J]. Front Physiol, 2019, 10: 1286. doi: 10.3389/fphys.2019.01286
    Chen L, Yin Z, Qin X, et al. CD74 ablation rescues type 2 diabetes mellitus-induced cardiac remodeling and contractile dysfunction through pyroptosis-evoked regulation of ferroptosis[J]. Pharmacol Res, 2022, 176: 106086. doi: 10.1016/j.phrs.2022.106086
    Yang M, Zheng J, Miao Y, et al. Serum-glucocorticoid regulated kinase 1 regulates alternatively activated macrophage polarization contributing to angiotensin II-induced inflammation and cardiac fibrosis[J]. Arterioscler Thromb Vasc Biol, 2012, 32(7): 1675–1686. doi: 10.1161/ATVBAHA.112.248732
    Gan W, Ren J, Li T, et al. The SGK1 inhibitor EMD638683, prevents Angiotensin II-induced cardiac inflammation and fibrosis by blocking NLRP3 inflammasome activation[J]. Biochim Biophys Acta Mol Basis Dis, 2018, 1864(1): 1–10. doi: 10.1016/j.bbadis.2017.10.001
    Wang J, Deng B, Liu J, et al. Xinyang Tablet inhibits MLK3-mediated pyroptosis to attenuate inflammation and cardiac dysfunction in pressure overload[J]. J Ethnopharmacol, 2021, 274: 114078. doi: 10.1016/j.jep.2021.114078
    Ma S, Feng J, Lin X, et al. Nicotinamide riboside alleviates cardiac dysfunction and remodeling in pressure overload cardiac hypertrophy[J]. Oxid Med Cell Longev, 2021, 2021: 5546867. doi: 10.1155/2021/5546867
    Zhao M, Zhang J, Xu Y, et al. Selective inhibition of NLRP3 inflammasome reverses pressure overload-induced pathological cardiac remodeling by attenuating hypertrophy, fibrosis, and inflammation[J]. Int Immunopharmacol, 2021, 99: 108046. doi: 10.1016/j.intimp.2021.108046
    Willeford A, Suetomi T, Nickle A, et al. CaMKIIδ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis[J]. JCI Insight, 2018, 3(12): e97054. doi: 10.1172/jci.insight.97054
    Heijman J, Muna AP, Veleva T, et al. Atrial myocyte NLRP3/CaMKII nexus forms a substrate for postoperative atrial fibrillation[J]. Circ Res, 2020, 127(8): 1036–1055. doi: 10.1161/CIRCRESAHA.120.316710
    Miller SA, Kolpakov MA, Guo X, et al. Intracardiac administration of neutrophil protease cathepsin G activates noncanonical inflammasome pathway and promotes inflammation and pathological remodeling in non-injured heart[J]. J Mol Cell Cardiol, 2019, 134: 29–39. doi: 10.1016/j.yjmcc.2019.06.016
    Li X, Zhu Q, Wang Q, et al. Protection of sacubitril/valsartan against pathological cardiac remodeling by inhibiting the NLRP3 inflammasome after relief of pressure overload in mice[J]. Cardiovasc Drugs Ther, 2020, 34(5): 629–640. doi: 10.1007/s10557-020-06995-x
    Wang J, Deng B, Liu Q, et al. Pyroptosis and ferroptosis induced by mixed lineage kinase 3 (MLK3) signaling in cardiomyocytes are essential for myocardial fibrosis in response to pressure overload[J]. Cell Death Dis, 2020, 11(7): 574. doi: 10.1038/s41419-020-02777-3
    Zhou J, Tian G, Quan Y, et al. Inhibition of P2X7 purinergic receptor ameliorates cardiac fibrosis by suppressing NLRP3/IL-1β pathway[J]. Oxid Med Cell Longev, 2020, 2020: 7956274. doi: 10.1155/2020/7956274
    Lu B, Xie J, Fu D, et al. Huoxue Qianyang Qutan recipe attenuates cardiac fibrosis by inhibiting the NLRP3 inflammasome signalling pathway in obese hypertensive rats[J]. Pharm Biol, 2021, 59(1): 1043–1055. doi: 10.1080/13880209.2021.1953541
    Lv S, Zeng Z, Gan W, et al. Lp-PLA2 inhibition prevents Ang II-induced cardiac inflammation and fibrosis by blocking macrophage NLRP3 inflammasome activation[J]. Acta Pharmacol Sin, 2021, 42(12): 2016–2032. doi: 10.1038/s41401-021-00703-7
    Li F, Zhang H, Yang L, et al. NLRP3 deficiency accelerates pressure overload-induced cardiac remodeling via increased TLR4 expression[J]. J Mol Med (Berl), 2018, 96(11): 1189–1202. doi: 10.1007/s00109-018-1691-0
    Gao Y, Tong G, Zhang X, et al. Interleukin-18 levels on admission are associated with mid-term adverse clinical events in patients with ST-segment elevation acute myocardial infarction undergoing percutaneous coronary intervention[J]. Int Heart J, 2010, 51(2): 75–81. doi: 10.1536/ihj.51.75
    El-Mesallamy HO, Hamdy NM, El-Etriby AK, et al. Plasma granzyme B in ST elevation myocardial infarction versus non-ST elevation acute coronary syndrome: comparisons with IL-18 and fractalkine[J]. Mediators Inflamm, 2013, 2013: 343268. doi: 10.1155/2013/343268
    Hartford M, Wiklund O, Hultén LM, et al. Interleukin-18 as a predictor of future events in patients with acute coronary syndromes[J]. Arterioscler Thromb Vasc Biol, 2010, 30(10): 2039–2046. doi: 10.1161/ATVBAHA.109.202697
    Ji Q, Zeng Q, Huang Y, et al. Elevated plasma IL-37, IL-18, and IL-18BP concentrations in patients with acute coronary syndrome[J]. Mediators Inflamm, 2014, 2014: 165742. doi: 10.1155/2014/165742
    Xie S, Chen Y, Zhang H, et al. Interleukin 18 and extracellular matrix metalloproteinase inducer cross-regulation: implications in acute myocardial infarction[J]. Transl Res, 2015, 165(3): 387–395. doi: 10.1016/j.trsl.2014.09.001
    Åkerblom A, James SK, Lakic TG, et al. Interleukin-18 in patients with acute coronary syndromes[J]. Clin Cardiol, 2019, 42(12): 1202–1209. doi: 10.1002/clc.23274
    Wang X, Cai X, Chen L, et al. The evaluation of plasma and leukocytic IL-37 expression in early inflammation in patients with acute ST-segment elevation myocardial infarction after PCI[J]. Mediators Inflamm, 2015, 2015: 626934. doi: 10.1155/2015/626934
    Pudil R, Pidrman V, Krejsek J, et al. Cytokines and adhesion molecules in the course of acute myocardial infarction[J]. Clin Chim Acta, 1999, 280(1–2): 127–134,doi: 10.1016/s0009-8981(98)00179-x.
    Ørn S, Ueland T, Manhenke C, et al. Increased interleukin-1β levels are associated with left ventricular hypertrophy and remodelling following acute ST segment elevation myocardial infarction treated by primary percutaneous coronary intervention[J]. J Intern Med, 2012, 272(3): 267–276. doi: 10.1111/j.1365-2796.2012.02517.x
    Hermansson C, Lundqvist A, Wasslavik C, et al. Reduced expression of NLRP3 and MEFV in human ischemic heart tissue[J]. Biochem Biophys Res Commun, 2013, 430(1): 425–428. doi: 10.1016/j.bbrc.2012.11.070
    Raleigh JV, Mauro AG, Devarakonda T, et al. Reperfusion therapy with recombinant human relaxin-2 (Serelaxin) attenuates myocardial infarct size and NLRP3 inflammasome following ischemia/reperfusion injury via eNOS-dependent mechanism[J]. Cardiovasc Res, 2017, 113(6): 609–619. doi: 10.1093/cvr/cvw246
    Lei Q, Yi T, Chen C. NF-κB-gasdermin D (GSDMD) axis couples oxidative stress and NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome-mediated cardiomyocyte pyroptosis following myocardial infarction[J]. Med Sci Monit, 2018, 24: 6044–6052. doi: 10.12659/MSM.908529
    Yu Y, Jin L, Zhuang Y, et al. Cardioprotective effect of rosuvastatin against isoproterenol-induced myocardial infarction injury in rats[J]. Int J Mol Med, 2018, 41(6): 3509–3516. doi: 10.3892/ijmm.2018.3572
    Euler DE, Hughes PJ, Scanlon PJ. Comparison of the effects of acute and chronic beta-blockade on infarct size in the dog after circumflex occlusion[J]. Cardiovasc Drugs Ther, 1988, 2(2): 231–238. doi: 10.1007/BF00051239
    Yu W, Jin G, Zhang J, et al. Selective activation of cannabinoid receptor 2 attenuates myocardial infarction via suppressing NLRP3 inflammasome[J]. Inflammation, 2019, 42(3): 904–914. doi: 10.1007/s10753-018-0945-x
    Cui Q, Wang J, Liu X, et al. Knockout of PTEN improves cardiac function and inhibits NLRP3-mediated cardiomyocyte pyroptosis in rats with myocardial ischemia-reperfusion[J]. Chin J Cell Mol Immunol (in Chinese), 2020, 36(3): 205–211.
    Song MS, Salmena L, Pandolfi PP. The functions and regulation of the PTEN tumour suppressor[J]. Nat Rev Mol Cell Biol, 2012, 13(5): 283–296. doi: 10.1038/nrm3330
    Han Y, Sun W, Ren D, et al. SIRT1 agonism modulates cardiac NLRP3 inflammasome through pyruvate dehydrogenase during ischemia and reperfusion[J]. Redox Biol, 2020, 34: 101538. doi: 10.1016/j.redox.2020.101538
    Yao L, Song J, Meng X, et al. Periostin aggravates NLRP3 inflammasome-mediated pyroptosis in myocardial ischemia-reperfusion injury[J]. Mol Cell Probes, 2020, 53: 101596. doi: 10.1016/j.mcp.2020.101596
    Climent M, Viggiani G, Chen Y, et al. MicroRNA and ROS crosstalk in cardiac and pulmonary diseases[J]. Int J Mol Sci, 2020, 21(12): 4370. doi: 10.3390/ijms21124370
    Lou Y, Wang S, Qu J, et al. miR-424 promotes cardiac ischemia/reperfusion injury by direct targeting of CRISPLD2 and regulating cardiomyocyte pyroptosis[J]. Int J Clin Exp Pathol, 2018, 11(7): 3222–3235.
    Ding S, Liu D, Wang L, et al. Inhibiting microRNA-29a protects myocardial ischemia-reperfusion injury by targeting SIRT1 and suppressing oxidative stress and NLRP3-mediated pyroptosis pathway[J]. J Pharmacol Exp Ther, 2020, 372(1): 128–135. doi: 10.1124/jpet.119.256982
    Lin J, Lin H, Ma C, et al. MiR-149 aggravates pyroptosis in myocardial ischemia-reperfusion damage via silencing FoxO3[J]. Med Sci Monit, 2019, 25: 8733–8743. doi: 10.12659/MSM.918410
    Zhou Y, Li K, Liu L, et al. MicroRNA-132 promotes oxidative stress-induced pyroptosis by targeting sirtuin 1 in myocardial ischaemia-reperfusion injury[J]. Int J Mol Med, 2020, 45(6): 1942–1950. doi: 10.3892/ijmm.2020.4557
    Dai Y, Wang S, Chang S, 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
    Wei X, Peng H, Deng M, et al. MiR-703 protects against hypoxia/reoxygenation-induced cardiomyocyte injury via inhibiting the NLRP3/caspase-1-mediated pyroptosis[J]. J Bioenerg Biomembr, 2020, 52(3): 155–164. doi: 10.1007/s10863-020-09832-w
    Yellon DM, Downey JM. Preconditioning the myocardium: from cellular physiology to clinical cardiology[J]. Physiol Rev, 2003, 83(4): 1113–1151. doi: 10.1152/physrev.00009.2003
    Heusch G. Molecular basis of cardioprotection: signal transduction in ischemic pre-, post-, and remote conditioning[J]. Circ Res, 2015, 116(4): 674–699. doi: 10.1161/CIRCRESAHA.116.305348
    Heusch G. Myocardial ischaemia-reperfusion injury and cardioprotection in perspective[J]. Nat Rev Cardiol, 2020, 17(12): 773–789. doi: 10.1038/s41569-020-0403-y
    Gou X, Xu D, Li F, et al. Pyroptosis in stroke-new insights into disease mechanisms and therapeutic strategies[J]. J Physiol Biochem, 2021, 77(4): 511–529. doi: 10.1007/s13105-021-00817-w
    Shi J, Tang M, Zhou S, et al. Programmed cell death pathways in the pathogenesis of idiopathic inflammatory myopathies[J]. Front Immunol, 2021, 12: 783616. doi: 10.3389/fimmu.2021.783616
    Woo Y, Lee HJ, Jung YM, et al. Regulated necrotic cell death in alternative tumor therapeutic strategies[J]. Cells, 2020, 9(12): 2709. doi: 10.3390/cells9122709
    Gong T, Liu L, Jiang W, et al. DAMP-sensing receptors in sterile inflammation and inflammatory diseases[J]. Nat Rev Immunol, 2020, 20(2): 95–112. doi: 10.1038/s41577-019-0215-7
    Zhang X, Qu H, Yang T, et al. Regulation and functions of NLRP3 inflammasome in cardiac fibrosis: current knowledge and clinical significance[J]. Biomed Pharmacother, 2021, 143: 112219. doi: 10.1016/j.biopha.2021.112219
    Song Z, Gong Q, Guo J. Pyroptosis: mechanisms and links with fibrosis[J]. Cells, 2021, 10(12): 3509. doi: 10.3390/cells10123509
    Wang C, Zhu L, Yuan W, et al. Diabetes aggravates myocardial ischaemia reperfusion injury via activating Nox2-related programmed cell death in an AMPK-dependent manner[J]. J Cell Mol Med, 2020, 24(12): 6670–6679. doi: 10.1111/jcmm.15318
    Wang X, Pan J, Liu H, et al. AIM2 gene silencing attenuates diabetic cardiomyopathy in type 2 diabetic rat model[J]. Life Sci, 2019, 221: 249–258. doi: 10.1016/j.lfs.2019.02.035
    Shen S, He F, Cheng C, et al. Uric acid aggravates myocardial ischemia-reperfusion injury via ROS/NLRP3 pyroptosis pathway[J]. Biomed Pharmacother, 2021, 133: 110990. doi: 10.1016/j.biopha.2020.110990
    Wu A, Sun W, Mou F. lncRNA-MALAT1 promotes high glucose-induced H9C2 cardiomyocyte pyroptosis by downregulating miR-141-3p expression[J]. Mol Med Rep, 2021, 23(4): 259. doi: 10.3892/mmr.2021.11898
    Wang X, Lian Z, Ge Y, et al. TRIM25 rescues against doxorubicin-Induced pyroptosis through promoting NLRP1 ubiquitination[J]. Cardiovasc Toxicol, 2021, 21(10): 859–868. doi: 10.1007/s12012-021-09676-9
    Li Y, Wang Y, Guo H, et al. IRF2 contributes to myocardial infarction via regulation of GSDMD induced pyroptosis[J]. Mol Med Rep, 2022, 25(2): 40. doi: 10.3892/mmr.2021.12556
    Yang F, Qin Y, Wang Y, et al. Metformin inhibits the NLRP3 inflammasome via AMPK/mTOR-dependent effects in diabetic cardiomyopathy[J]. Int J Biol Sci, 2019, 15(5): 1010–1019. doi: 10.7150/ijbs.29680
    Liu J, Li Y, Yang M, et al. SP1-induced ZFAS1 aggravates sepsis-induced cardiac dysfunction via miR-590-3p/NLRP3-mediated autophagy and pyroptosis[J]. Arch Biochem Biophys, 2020, 695: 108611. doi: 10.1016/j.abb.2020.108611
    Huang C, Andres AM, Ratliff EP, et al. Preconditioning involves selective mitophagy mediated by parkin and p62/SQSTM1[J]. PLoS One, 2011, 6(6): e20975. doi: 10.1371/journal.pone.0020975
    Sun W, Lu H, Dong S, et al. Beclin1 controls caspase-4 inflammsome activation and pyroptosis in mouse myocardial reperfusion-induced microvascular injury[J]. Cell Commun Signal, 2021, 19(1): 107. doi: 10.1186/s12964-021-00786-z
    Wang Y, Jasper H, Toan S, et al. Mitophagy coordinates the mitochondrial unfolded protein response to attenuate inflammation-mediated myocardial injury[J]. Redox Biol, 2021, 45: 102049. doi: 10.1016/j.redox.2021.102049
    Chang X, Lochner A, Wang HH, et al. Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control[J]. Theranostics, 2021, 11(14): 6766–6785. doi: 10.7150/thno.60143
    Zhou H, Ren J, Toan S, et al. Role of mitochondrial quality surveillance in myocardial infarction: from bench to bedside[J]. Ageing Res Rev, 2021, 66: 101250. doi: 10.1016/j.arr.2020.101250
    Wang J, Zhou H. Mitochondrial quality control mechanisms as molecular targets in cardiac ischemia-reperfusion injury[J]. Acta Pharm Sin B, 2020, 10(10): 1866–1879. doi: 10.1016/j.apsb.2020.03.004
    Qiu Y, Ma Y, Jiang M, et al. Melatonin alleviates LPS-induced pyroptotic cell death in human stem cell-derived cardiomyocytes by activating autophagy[J]. Stem Cells Int, 2021, 2021: 8120403. doi: 10.1155/2021/8120403
    Guo R, Wang H, Cui N. Autophagy regulation on pyroptosis: mechanism and medical implication in sepsis[J]. Mediators Inflamm, 2021, 2021: 9925059. doi: 10.1155/2021/9925059
    Chang P, Li H, Hu H, et al. The role of HDAC6 in autophagy and NLRP3 inflammasome[J]. Front Immunol, 2021, 12: 763831. doi: 10.3389/fimmu.2021.763831
  • 加载中


    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索


    Article Metrics

    Article views (68) PDF downloads(4) Cited by()
    Proportional views


    DownLoad:  Full-Size Img  PowerPoint