Progression in the study of the Toll/NF-κB and MAPK signaling pathways in sepsis cardiomyopathy
-
Abstract: Sepsis is a systemic inflammatory response syndrome caused by the interaction between the host's immune system and invading pathogens.Severe cases can develop severe sepsis and septic shock.Sepsis cardiomyopathy is a reversible cardiac dysfunction characterized by enlarged left ventricle and decreased ejection fraction which can complete return to normal in 7-10 days.It is common in patients with severe sepsis and is the main cause of death.Although the exact mechanism by which sepsis causes cardiac dysfunction is unclear,TLRs act as immunomodulators to regulate specific signaling pathways during the immune response and play an important role in myocardial suppression caused by sepsis cardiomyopathy.Now relevant researches were reviewed.
-
[1] Singer M,Deutschman CS,Seymour CW,et al.The Third International Consensus Definitions for Sepsis and Septic Shock(Sepsis-3)[J].JAMA,2016,315(8):801-810.
[2] Jeong HS,Lee TH,Bang CH,et al.Risk factors and outcomes of sepsis-induced myocardial dysfunction and stress-induced cardiomyopathy in sepsis or septic shock:A comparative retrospective study[J].Medicine,2018,97(13):e0263.
[3] Liu YC,Yu MM,Shou ST,et al.Sepsis-Induced Cardiomyopathy:Mechanisms and Treatments[J].Front Immunol,2017,8:1021.
[4] Kong W,Kang K,Gao Y,et al.Dexmedetomidine alleviates LPS-induced septic cardiomyopathy via the cholinergic anti-inflammatory pathway in mice[J].Am J Transl Res,2017,9(11):5040-5047.
[5] Achek A,Yesudhas D,Choi S.Toll-like receptors:promising therapeutic targets for inflammatory diseases[J].Arch Pharm Res,2016,39(8):1032-1049.
[6] Parker MM,Shelhamer JH,Bacharach L,et al.Profound but reversible myocardial depression in patients with septic shock[J].Ann Intern Med,1984,100(4):483-490.
[7] Zeng XM,Liu DH,Han Y,et al.Assessment of inflammatory markers and mitochondrial factors in a rat model of sepsis-induced myocardial dysfunction[J].Am J Transl Res,2020,12(3):901-911.
[8] Prescott HC,Angus DC.Enhancing Recovery From Sepsis:A Review[J].JAMA,2018,319(1):62-75.
[9] Walley KR.Sepsis-induced myocardial dysfunction[J].Curr Opin Crit Care,2018,24(4):292-299.
[10] 向仕钊,李金,杨梁.脓毒症心肌病研究进展[J].中华心力衰竭和心肌病杂志(中英文),2019,3(1):59-61.
[11] Geraci G,Buccheri D,Zanoli L,et al.Renal haemodynamics and coronary atherosclerotic burden are associated in patients with hypertension and mild coronary artery disease[J].Exp Ther Med,2019,17(4):3255-3263.
[12] Ramphul K,Mejias SG,Sombans S,et al.Cardiac arrhythmias associated with Takotsubo cardiomyopathy and ST-segment Elevation Myocardial Infarction(STEMI)[J].Am J Cardiol,2020,S0002-9149(20):30370-30372.
[13] Ghadri JR,Wittstein IS,Prasad A,et al.International Expea Consensus Document on Takotsubo Syndrome(Panll):Diagnostic Workup,Outcome,and Management[J].Eur Heart J,2018,39(22):2047-2062.
[14] Garg AD,Agostinis P.Cell death and immunity in cancer:From danger signals to mimicry of pathogen defense responses[J].Immunol Rev,2017,280(1):126-148.
[15] Epelman S,Liu PP,Mann DL.Role of innate and adaptive immune mechanisms in cardiac injury and repair[J].Nat Rev Immunol,2015,15(2):117-129.
[16] Yu L,Feng Z.The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure[J].Mediators Inflamm,2018,2018:9874109.
[17] Aarts S,Seijkens T,Kusters P,et al.Inhibition of CD40-TRAF6 interactions by the small molecule inhibitor 6877002 reduces neuroinflammation[J].J Neuroinflammation,2017,14(1):105.
[18] Chen G,Gao X,Wang J,et al.Hypoxia-induced microRNA-146a represses Bcl-2 through Traf6/IRAK1 but not Smad4 to promote chondrocyte autophagy[J].Biol Chem,2017,398(4):499-507.
[19] Yang Y,Lv J,Jiang S,et al.The emerging role of Toll-like receptor 4 in myocardial inflammation[J].Cell Death Dis,2016,7(5):e2234.
[20] Masahiro Y,Shintaro S,Hiroaki H,et al.Role of Adaptor TRIF in the MyD88-Independent Toll-like Receptor Signaling Pathway[J].Science,2003,301(5633):640-643.
[21] Abdullah M,Berthiaume JM,Willis MS.Tumor necrosis factor receptor-associated factor 6 as a nuclear factor kappa B-modulating therapeutic target in cardiovascular diseases:at the heart of it all[J].Transl Res,2018,195:48-61.
[22] Li M,Liu J,Bi Y,et al.Potential Medications or Compounds Acting on Toll-like Receptors in Cerebral Ischemia[J].Curr Neuropharmacol,2018,16(2):160-175.
[23] Na YR,Je S,Seok SH.Metabolic features of macrophages in inflammatory diseases and cancer[J].Cancer Lett,2018,28(413):46-58.
[24] Wang W,Deng Z,Wu H,et al.A small secreted protein triggers a TLR2/4-dependent inflammatory response during invasive Candida albicans infection[J].Nat Commun,2019,10(1):1015.
[25] Zarember KA,Godowski PJ.Tissue expression of human Toll-like receptors and differential regulation of Toll-like receptor mRNAs in leukocytes in response to microbes,their products,and cytokines.Immunol[J].2002,168(2):554-561.
[26] Spurthi KM,Sarikhani M,Mishra S,et al.Toll-like receptor 2 deficiency hyperactivates the FoxO1 transcription factor and induces aging-associated cardiac dysfunction in mice[J].J Biol Chem,2018,293(34):13073-13089.
[27] Knuefermann P,Sakata Y,Baker JS,et al.Toll-like receptor 2 mediates Staphylococcus aureus-induced myocardial dysfunction and cytokine production in the heart[J].Circulation,2004,110:3693-3698.
[28] Ha TZ,Lu C,Liu L,et al.TLR2 ligands attenuate cardiac dysfunction in polymicrobial sepsis via a phosphoinositide 3-kinase-dependent mechanism[J].Am J Physiol Heart Circ Physiol,2010,298:H984-H991.
[29] 郭予涛,阳娟林,明祥.Toll样受体3在脓毒症并心功能障碍患儿中的表达及意义[J].国际医药卫生导报,2018,24(10):1498-1501.
[30] Gao ML,Wu KC,Deng WL,et al.Toll-like receptor 3 activation initiates photoreceptor cell death in vivo and in vitro[J].Invest Ophthalmol Vis Sci,2017,58(2):801-811.
[31] Gao ML,Ha T,Zhang X,et al.Toll-like receptor 3 plays a central role in cardiac dysfunction during polymicrobial sepsis[J].Crit Care Med,2012,40(8):2390-2399.
[32] Fattahi F,Russell MW,Malan EA,et al.Harmful Roles of TLR3 and TLR9 in Cardiac Dysfunction Developing during Polymicrobial Sepsis[J].Biomed Res Int,2018,30(2018):4302726.
[33] Su Q,Li L,Sun Y,et al.Effects of the TLR4/Myd88/NF-κB Signaling Pathway on NLRP3 Inflammasome in Coronary Microembolization-Induced Myocardial Injury[J].Cell Physiol Biochem,2018,47(4):1497-1508.
[34] Zhou D,Zhu Y,Ouyang MZ,et al.Knockout of toll-like receptor 4 improves survival and cardiac function in a murine model of severe sepsis[J].Mol Med Rep,2018,17:5368-5375.
[35] Xie J,Zhang L,Fan X,et al.MicroRNA-146a improves sepsis-induced cardiomyopathy by regulating the TLR-4/NF-κB signaling pathway[J].Exp Ther Med,2019,18(1):779-785.
[36] Liu X,Wen M,Li X,et al.β1 receptor blocker decreases the myocardial inflammation in the sepsis adult rats through inhibition of TLR4/NF-ΚB signaling pathway[J].Zhonghua Wei Zhong Bing Ji Jiu Yi Xue,2019,31(2):193-197.
[37] Leliefeld PH,Wessels CM,Leenen LP,et al.The role of neutrophils in immune dysfunction during severe inflammation[J].Crit Care,2016,20:73.
[38] Hobai IA,Morse JC,Siwik DA,et al.Lipopolysaccharide and cytokines inhibit rat cardiomyocyte contractility in vitro[J].J Surg Res,2015,193:888-901.
[39] Gao M,Wang X,Zhang X,et al.Attenuation of cardiac dysfunction in polymicrobial sepsis by microRNA-146a is mediated via targeting of IRAK1 and TRAF6 expression[J].J Immunol,2015,195(2):672-682.
[40] Sun LJ,Qiao W,Xiao YJ,et al.Naringin mitigates myocardial strain and the inflammatory response in sepsis-induced myocardial dysfunction through regulation of PI3K/AKT/NF-κB pathway[J].Int Immunopharmacol,2019,75:105782.
[41] Zhai J,Guo Y.Paeoniflorin attenuates cardiac dysfunction in endotoxemic mice via the inhibition of nuclear factor-kappaB[J].Biomed Pharmacother,2016,80:200-206.
[42] Kakihana Y,Ito T,Nakahara M,et al.Sepsis-induced myocardial dysfunction:pathophysiology and management[J].J Intensive Care,2016,4(1):22.
[43] Li H,Xing Y,Yang D,et al.Alpha-1 Adrenergic Receptor Agonist Phenylephrine Inhibits Sepsis-Induced Cardiomyocyte Apoptosis and Cardiac Dysfunction via Activating ERK1/2 Signal Pathway[J].Shock,2019,52(1):122-133.
[44] Yousif NG,Hadi NR,Al-Amran F,et al.Cardioprotective effects of irbesartan in polymicrobial sepsis:The role of the p38 MAPK/NF-κB signaling pathway[J].Herz,2018,43(2):140-145.
[45] Zhang T,Yin YC,Ji X,et al.AT1R knockdown confers cardioprotection against sepsis-induced myocardial injury by inhibiting the MAPK signaling pathway in rats[J].J Cell Biochem,2020,121(1):25-42.
计量
- 文章访问数: 310
- PDF下载数: 49
- 施引文献: 0