HMGB1与动脉粥样硬化相关疾病的研究进展
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摘要
高迁移率族蛋白B1 (HMGB1)是真核生物普遍表达的一种非组蛋白核因子。在致病因素作用下,HMGB1通过主动和被动释放,与晚期糖基化终末产物受体和Toll样等受体相互作用,引起炎症介质释放并激发机体的免疫炎症反应。HMGB1可能通过诱导白细胞的浸润、血小板的黏附聚集以及血管平滑肌细胞的迁移促进肺动脉高压、冠心病、缺血性脑卒中等多种动脉粥样硬化相关疾病发生和进展。与此同时,HMGB1在某些情况下还能产生特定的生物学效应来减轻上述一些疾病中机体的损伤。然而,该作用产生的详细机制目前尚不清晰,许多问题还有待深入探讨。
High mobility group box 1( HMGB1) is a kind of a non-histone nuclear factor identified as commonly expressed in eucaryotes. Through active and passive releasing,it interacts with receptor for advanced glycation end products and Toll-like receptors,causing the release of inflammatory mediators and stimulating the immune inflammatory response of the body under the damage of the pathogenic factors. HMGB1 may promote the generation and progression of atherosclerotic diseases such as pulmonary arterial hypertension,coronary heart disease,ischemic stroke,via promoting the infiltration of white blood cells,platelet adhesion and aggregation,and the migration of vascular smooth muscle cells. At the same time,HMGB1 can also produce certain biological effects to alleviate the damage of the body in some diseases mentioned above.However,the detailed mechanism of this effect is not clear at present,and many problems still require to be further discussed.
High mobility group box 1( HMGB1) is a kind of a non-histone nuclear factor identified as commonly expressed in eucaryotes. Through active and passive releasing,it interacts with receptor for advanced glycation end products and Toll-like receptors,causing the release of inflammatory mediators and stimulating the immune inflammatory response of the body under the damage of the pathogenic factors. HMGB1 may promote the generation and progression of atherosclerotic diseases such as pulmonary arterial hypertension,coronary heart disease,ischemic stroke,via promoting the infiltration of white blood cells,platelet adhesion and aggregation,and the migration of vascular smooth muscle cells. At the same time,HMGB1 can also produce certain biological effects to alleviate the damage of the body in some diseases mentioned above.However,the detailed mechanism of this effect is not clear at present,and many problems still require to be further discussed.
引文
[1] Andersson U, Erlandsson-Harris H,Yang H,et al. HMGB1 as a DNA-binding cytokine[J]. Leukoc Biol, 2002, 72(6):1084-4091.
[2] Wang H, Yang H, Tracey KJ. Extracellular role of HMGB1 in inflammation and sepsis[J]. J Intern Med, 2004, 255(3):320-331.
[3] Kalinina N, Agrotis A, Antropov Y, et al. Increased expression of the DNA-binding cytokine HMGB1 in human atherosclerotic lesions:Role of activated macrophages and cytokines[J]. Arterioscler Thromb Vase Biol,2004,24:2320-2325.
[4] Sadamura-Takenaka Y, Ito T, Noma S,et al. HMGB1 promotes the development of pulmonary arterial hypertension in rats[J]. PLoSOne,2014,9(7):e102482.
[5] Goodwin GH, Sanders C, Johns EW. A new group of chromatinassociated proteins with a high content of acidic and basic amino acids[J].Eur J Biochem, 1973,38(1):1449.
[6] Huan CC, Wang HX,Sheng XX, et al. Porcine epidemic diarrhea virus nucleoprotein contributes to HMGB1 transcription and release by interacting with C/EBP-β[J]. Oncotarget,2016,7(46):75064-75080.
[7] He M,Bianchi ME,Coleman TR,et al. Exploring the biological functional mechanism of the HMGB1/TLR4/MD-2 complex by surface plasmon resonance[J]. Mol Med,2018,24(1):21.
[8] Yang L, Wang F, Yang L, et al. HMGB1 a-Box reverses brain edema and deterioration of neurological function in a traumatic brain injury mouse model[J]. Cell Physiol Biochem,2018,46(6):2532-2542.
[9] Bandala-Sanchez E,G Bediaga N,Goddard-Borger ED, et al.CD52 glycan binds the proinflammatory B box of HMGB1 to engage the Siglec-10 receptor and suppress human T cell function[J]. Proc Natl Acad Sci U S A,2018,115(30):7783-7788.
[10] Aucott H,Sowinska A,Harris HE,et al. Ligation of free HMGB1to TLR2 in the absence of ligand is negatively regulated by the C-terminal tail domain[J]. Mol Med,2018,24(1):19.
[11] Erlandsson HH, Andersson U. Mini-review:The nuclear protein HMGB1 as a proinflammatory mediator[J]. Eur J Immunol,2004,34(6):15034512.
[12] Park EJ,Kim YM,Kim HJ,et al. Degradation of histone deacetylase 4 via the TLR4/JAK/STATI signaling pathway promotes the acetylation of high mobility group box 1(HMGB1)in lipopolysaccharide-activated macrophages[J]. FEBS Open Bio,2018,8(7):1119-1126.
[13] Amato J, Madanayake TW, Iaccarino N, et al. HMGB1 binds to the KRAS promoter G-quadruplex:A new player in oncogene transcriptional regulation?[J]. Chem Commun(Camb),2018,54(68):9442-9445.
[14] Funayama A, Shishido T, Netsu S, et al. Cardiac nuclear high mobility group box 1 prevents the development of cardiac hypertrophy and heart failure[J]. Cardiovasc Res,2013, 99(4):657-664.
[15] Bianchi ME,Beltrame M. Upwardly mobile proteins. Workshop:The role of HMG proteins in chromatin structure, gene expression and neoplasia[J]. EMBO Rep,2000,1(2):109-114.
[16] Xie X,Zhu T,Chen L,et al. MCPIP1-induced autophagy mediates ischemia/reperfusion injury in endothelial cells via HMGB1 and CaSR[J].Sci Rep,2018,8(1):1735.
[17] Kim EJ, Park SY, Baek SE,et al. HMGBI Increases IL-1βProduction in Vascular Smooth Muscle Cells via NLRP3 Inflammasome[J]. Front Physiol,2018,9:313.
[18] Taguchi A, Blood DC, del TG,et al. Blockade of RAGE-amphoterin signalling suppresses tumour growth and metastases[J].Nature,2000,405:354-360.
[19] Andersson U,Yang H,Harris H. High-mobility group box 1protein(HMGB1)operates as an alarmin outside as well as inside cells[J]. Semin Immunol,2018,38:40-48.
[20] Meng X,Chen M,Su W,et al. The differentiation of mesenchymal stem cells to vascular cells regulated by the HMGB1/RAGE axis:Its application in cell therapy for transplant arteriosclerosis[J].Stem Cell Res Ther,2018,9(1):85.
[21] Zhou H,Jin C,Cui L,et al. HMGB1 contributes to the irradiationinduced endothelial barrier injury through receptor for advanced glycation endproducts(RAGE)[J]. J Cell Physiol,2018, 233(9):6714-6721.
[22] Meng X,Su W,Tao X,et al. Oxidation prevents HMGB1 inhibition on PDGF-induced differentiation of multipotent vascular stem cells to smooth muscle cells:A possible mechanism linking oxidative stress to atherosclerosis[J]. Biomed Res Int,2018,2018:4019814.
[23] van Beijnum JR,Buurman WA,Griffioen AW. Convergence and amplification of toll-4ikereceptor(TLR)and receptor for advanced glycation end products(RAGE)signaling pathways via high mobility group B1(HMGB1)[J]. Angiogenesis, 2008,11(1):91-99.
[24] Morrell NW, Adnot S, Archer SL, et al. Cellular and molecular basis of pulmonary arterial hypertension[J]. J Am Coll Cardiol,2009,54:S20-31.
[25] Selejan SR,Linz D,Tatu AM,et al. Sympathoadrenergic suppression improves heart function by upregulating the ratio of sRAGE/RAGE in hypertension with metabolic syndrome[J]. J Mol Cell Cardiol, 2018,122:34-46.
[26] Zabini D,Crnkovic S,Xu H, et al. High-mobility group box-4induces vascular remodelling processes via c-Jun activation[J].J Cell Mol Med,2015,19(5):1151-4161.
[27] Li WJ,Hu K,Yang JP,et al. HMGB1 affects the development of pulmonary arterial hypertension via RAGE[J]. Eur Rev Med Pharmacol Sci,2017,21(17):3950-3958.
[28] Jia D, He Y, Zhu Q, et al. RAGE-mediated extracellular matrix proteins accumulation exacerbates HySu-induced pulmonary hypertension[J]. Cardiovasc Res,2017,113(6):586-597.
[29] Maugeri N, Rovere-Querini P, Baldini M, et al. Oxidative stress elicits platelet/leukocyte inflammatory interactions via HMGB1:A candidate for microvessel injury in sytemic sclerosis[J]. Antioxid Redox Signal,2014,20(7):10604 074.
[30] Bauer EM, Shapiro R, Billiar TR,et al. High mobility group Box 1inhibits human pulmonary artery endothelial cell migration via a Toll-4ike receptor-4 and interferon response factor 3-dependent mechanism(s)[J]. J Biol Chem,2013,288(2):1365-1373.
[31] Nogueira-Ferreira R, Ferreira-Pinto MJ, Silva AF, et al. HMGB1down-regulation mediates terameprocol vascular anti-proliferative effect in experimental pulmonary hypertension[J]. J Cell Physiol,2017,232(11):3128-3138.
[32] Yang PS, Kim DH, Lee YJ, et al. Glycyrrhizin, inhibitor of high mobility group box-4, attenuates monocrotaline-induced pulmonary hypertension and vascular remodeling in rats[J]. Respir Res,2014,15:148.
[33] Wang JS,Sheu WH,Lee WJ,et al. Levels of serum high mobility group box 1 were independently associated with cardiovascular risk in patients undergoing coronary angiography[J]. Clin Chim Acta,2018,483:130 4 34.
[34] Yao HC,Zhao AP,Han QF,et al. Correlation between serum highmobility group box4 levels and high-sensitivity C-reactive protein and troponin I in patients with coronary artery disease[J]. Exp Ther Med,2013,6(1):121424.
[35] Huang YY, Su W, Zhu ZW, et al. Elevated serum HMGB1 in pulmonary arterial hypertension secondary to congenital heart disease[J]. Vascul Pharmacol,2016,85:66-72.
[36] Andrassy M,Volz HC,Maack B,et al. HMGB1 is associated with atherosclerotic plaque composition and burden in patients with stable coronary artery disease[J]. PLoS One,2012,7(12):e52081.
[37] Karuppagounder V, Giridharan VV, Arumugam S,et al. Modulation of macrophage polarization and HMGB1-TLR2/TLR4 cascade plays a crucial role for cardiac remodeling in senescence-accelerated prone mice[J]. PLoS One,2016,11(4):e0152922.
[38] Wu RN, Yu TY, Zhou JC, et al. Targeting HMGB1 ameliorates cardiac fibrosis through restoring TLR2-mediated autophagy suppression in myocardial fibroblasts[J]. Int J Cardiol, 2018, 267:156-162.
[39] Ahrens I, Chen YC, Topcic D, et al. HMGB1 binds to activated platelets via the receptor for advanced glycation end products and is present in platelet rich human coronary artery thrombi[J].Thromb Haemost,2015,114(5):994-4003.
[40] Dozio E,Vianello E,Briganti S,et al. Expression of the receptor for advanced glycation end products in epicardial fat:Link with tissue thickness and local insulin resistance in coronary artery disease[J]. J Diabetes Res,2016,2016:2327341.
[41] Li Q,Li ZM,Sun SY,et al. PARP1 interacts with HMGB1 and promotes its nuclearexport in pathological myocardial hypertrophy[J/OL]. Acta Pharmacol Sin, 2018[2018-08-21]. https://www. nature. com/articles/s41401-018-0044-4.[publised online ahead of print July 20,2018].
[42] Yang J,Chen L, Yang J,et al. High mobility group box-4 induces migration of vascular smooth muscle cells via TLR4-dependent PI3K/Akt pathway activation[J]. Mol Biol Rep,2012,39(3):3361-3367.
[43] He YY, Wen Y, Zheng XN, et al. Intramyocardial delivery of HMGB1 by a novel thermosensitive hydrogel attenuates cardiac remodeling and improves cardiac functionafter myocardial infarction[J]. Cardiovasc Pharmacol,2013,61(4):283-290.
[44] Le K,Mo S,Lu X,et al. Association of circulating blood HMGB1levels with ischemic stroke:A systematic review and meta-analysis[J]. Neurol Res,2018,17:140.
[45]奥婷,张芹,肖淑英,许娜,等.HMGB1与缺血性脑卒中关系的研究进展[J].医学综述,2018,24(9):1681-1686.
[46] Richard SA,Sackey M,Su Z,et al. Pivotal neuroinflammatory and therapeutic role of high mobility group box 1 in ischemic stroke[J]. Biosci Rep,2017,37(6). pii:BSR20171104.
[47] Tian X,Liu C,Shu Z, et al. Review:Therapeutic targeting of HMGBI in stroke[J]. Curr Drug Deliv,2017,14(6):785-790.
[48] Shichita T, Hasegawa E, Kimura A,et al. Peroxiredoxin family proteins are key initiators of post-ischemic inflammation in the brain[J]. Nat Med,2012,18(6):911-917.
[49] Ooboshi H, Shichita T. DAMPs(damage-associated molecular patterns)and inflammation[J]. Nihon Rinsho, 2016,74(4):573-578.
[50] Zhang H, Xiong X, Liu J, et al. Emulsified isoflurane protects against transient focal cerebral ischemia injury in rats via the PI3K/Akt signaling pathway[J]. Anesth Analg,2016, 122(5):1377-1384.
[51] Choi JY,Kim BG. Toll-like receptor 2:A novel therapeutic target for ischemic white matter injury and oligodendrocyte death[J].Exp Neurobiol,2017,26(4):186494.
[52] Liu Y,Gao Y,Yang J,et al. MicroRNA-381 reduces inflammation and infiltration of macrophages in polymyositis via downregulating HMGB1[J]. Int J Oncol,2018,53(3):1332-1342.
[53] Zhan LY, Lei SQ, Zhaing BH, et al. Overexpression of miR-381relieves neuropathicpain development via targeting HMGB1 and CXCR4[J]. Biomed Pharmacother,2018,107:818-823.
[54] Hu J,Liu B, Zhao Q, et al. Bone marrow stromal cells inhibits HMGB1-mediated inflammation after stroke in type 2 diabetic rats[J]. Neuroscience,2016,324:11-19.
[55] Nakamura Y,Nakano T,Irie K,et al. Recombinant human soluble thrombomodulin ameliorates cerebral ischemic injury through a high-mobility group box 1 inhibitory mechanism without hemorrhagic complications in mice[J]. J Neurol Sci,2016,362:278-282.
[56] Ay L, Nasser R, Simon B, et al. Transcutaneous cervical vagus nerve stimulation ameliorates acute ischemic injury in rats[J].Brain Stimul,2016,9(2):166-473.
[57] Zhou S,Lu H,Chen R,et al. Angiotensin II enhances the acetylation and release of HMGB1 in RAW264. 7 macrophage[J/OL]. Cell Biol Int,2018[2018-08-17]. https://onlinelibrary.wiley. com/doi/abs/10. 1002/cbin.10984.[publised online ahead of print May 9,2018].
[58] Masson GS,Nair AR, Silva Soares PP,et al. Aerobic training normalizes autonomic dysfunction, HMGB1 content, microglia activation and inflammation in hypothalamic paraventricular nucleus of SHR[J]. Am J Physiol Heart Circ Physiol, 2015, 309(7):H1115-1122.
[2] Wang H, Yang H, Tracey KJ. Extracellular role of HMGB1 in inflammation and sepsis[J]. J Intern Med, 2004, 255(3):320-331.
[3] Kalinina N, Agrotis A, Antropov Y, et al. Increased expression of the DNA-binding cytokine HMGB1 in human atherosclerotic lesions:Role of activated macrophages and cytokines[J]. Arterioscler Thromb Vase Biol,2004,24:2320-2325.
[4] Sadamura-Takenaka Y, Ito T, Noma S,et al. HMGB1 promotes the development of pulmonary arterial hypertension in rats[J]. PLoSOne,2014,9(7):e102482.
[5] Goodwin GH, Sanders C, Johns EW. A new group of chromatinassociated proteins with a high content of acidic and basic amino acids[J].Eur J Biochem, 1973,38(1):1449.
[6] Huan CC, Wang HX,Sheng XX, et al. Porcine epidemic diarrhea virus nucleoprotein contributes to HMGB1 transcription and release by interacting with C/EBP-β[J]. Oncotarget,2016,7(46):75064-75080.
[7] He M,Bianchi ME,Coleman TR,et al. Exploring the biological functional mechanism of the HMGB1/TLR4/MD-2 complex by surface plasmon resonance[J]. Mol Med,2018,24(1):21.
[8] Yang L, Wang F, Yang L, et al. HMGB1 a-Box reverses brain edema and deterioration of neurological function in a traumatic brain injury mouse model[J]. Cell Physiol Biochem,2018,46(6):2532-2542.
[9] Bandala-Sanchez E,G Bediaga N,Goddard-Borger ED, et al.CD52 glycan binds the proinflammatory B box of HMGB1 to engage the Siglec-10 receptor and suppress human T cell function[J]. Proc Natl Acad Sci U S A,2018,115(30):7783-7788.
[10] Aucott H,Sowinska A,Harris HE,et al. Ligation of free HMGB1to TLR2 in the absence of ligand is negatively regulated by the C-terminal tail domain[J]. Mol Med,2018,24(1):19.
[11] Erlandsson HH, Andersson U. Mini-review:The nuclear protein HMGB1 as a proinflammatory mediator[J]. Eur J Immunol,2004,34(6):15034512.
[12] Park EJ,Kim YM,Kim HJ,et al. Degradation of histone deacetylase 4 via the TLR4/JAK/STATI signaling pathway promotes the acetylation of high mobility group box 1(HMGB1)in lipopolysaccharide-activated macrophages[J]. FEBS Open Bio,2018,8(7):1119-1126.
[13] Amato J, Madanayake TW, Iaccarino N, et al. HMGB1 binds to the KRAS promoter G-quadruplex:A new player in oncogene transcriptional regulation?[J]. Chem Commun(Camb),2018,54(68):9442-9445.
[14] Funayama A, Shishido T, Netsu S, et al. Cardiac nuclear high mobility group box 1 prevents the development of cardiac hypertrophy and heart failure[J]. Cardiovasc Res,2013, 99(4):657-664.
[15] Bianchi ME,Beltrame M. Upwardly mobile proteins. Workshop:The role of HMG proteins in chromatin structure, gene expression and neoplasia[J]. EMBO Rep,2000,1(2):109-114.
[16] Xie X,Zhu T,Chen L,et al. MCPIP1-induced autophagy mediates ischemia/reperfusion injury in endothelial cells via HMGB1 and CaSR[J].Sci Rep,2018,8(1):1735.
[17] Kim EJ, Park SY, Baek SE,et al. HMGBI Increases IL-1βProduction in Vascular Smooth Muscle Cells via NLRP3 Inflammasome[J]. Front Physiol,2018,9:313.
[18] Taguchi A, Blood DC, del TG,et al. Blockade of RAGE-amphoterin signalling suppresses tumour growth and metastases[J].Nature,2000,405:354-360.
[19] Andersson U,Yang H,Harris H. High-mobility group box 1protein(HMGB1)operates as an alarmin outside as well as inside cells[J]. Semin Immunol,2018,38:40-48.
[20] Meng X,Chen M,Su W,et al. The differentiation of mesenchymal stem cells to vascular cells regulated by the HMGB1/RAGE axis:Its application in cell therapy for transplant arteriosclerosis[J].Stem Cell Res Ther,2018,9(1):85.
[21] Zhou H,Jin C,Cui L,et al. HMGB1 contributes to the irradiationinduced endothelial barrier injury through receptor for advanced glycation endproducts(RAGE)[J]. J Cell Physiol,2018, 233(9):6714-6721.
[22] Meng X,Su W,Tao X,et al. Oxidation prevents HMGB1 inhibition on PDGF-induced differentiation of multipotent vascular stem cells to smooth muscle cells:A possible mechanism linking oxidative stress to atherosclerosis[J]. Biomed Res Int,2018,2018:4019814.
[23] van Beijnum JR,Buurman WA,Griffioen AW. Convergence and amplification of toll-4ikereceptor(TLR)and receptor for advanced glycation end products(RAGE)signaling pathways via high mobility group B1(HMGB1)[J]. Angiogenesis, 2008,11(1):91-99.
[24] Morrell NW, Adnot S, Archer SL, et al. Cellular and molecular basis of pulmonary arterial hypertension[J]. J Am Coll Cardiol,2009,54:S20-31.
[25] Selejan SR,Linz D,Tatu AM,et al. Sympathoadrenergic suppression improves heart function by upregulating the ratio of sRAGE/RAGE in hypertension with metabolic syndrome[J]. J Mol Cell Cardiol, 2018,122:34-46.
[26] Zabini D,Crnkovic S,Xu H, et al. High-mobility group box-4induces vascular remodelling processes via c-Jun activation[J].J Cell Mol Med,2015,19(5):1151-4161.
[27] Li WJ,Hu K,Yang JP,et al. HMGB1 affects the development of pulmonary arterial hypertension via RAGE[J]. Eur Rev Med Pharmacol Sci,2017,21(17):3950-3958.
[28] Jia D, He Y, Zhu Q, et al. RAGE-mediated extracellular matrix proteins accumulation exacerbates HySu-induced pulmonary hypertension[J]. Cardiovasc Res,2017,113(6):586-597.
[29] Maugeri N, Rovere-Querini P, Baldini M, et al. Oxidative stress elicits platelet/leukocyte inflammatory interactions via HMGB1:A candidate for microvessel injury in sytemic sclerosis[J]. Antioxid Redox Signal,2014,20(7):10604 074.
[30] Bauer EM, Shapiro R, Billiar TR,et al. High mobility group Box 1inhibits human pulmonary artery endothelial cell migration via a Toll-4ike receptor-4 and interferon response factor 3-dependent mechanism(s)[J]. J Biol Chem,2013,288(2):1365-1373.
[31] Nogueira-Ferreira R, Ferreira-Pinto MJ, Silva AF, et al. HMGB1down-regulation mediates terameprocol vascular anti-proliferative effect in experimental pulmonary hypertension[J]. J Cell Physiol,2017,232(11):3128-3138.
[32] Yang PS, Kim DH, Lee YJ, et al. Glycyrrhizin, inhibitor of high mobility group box-4, attenuates monocrotaline-induced pulmonary hypertension and vascular remodeling in rats[J]. Respir Res,2014,15:148.
[33] Wang JS,Sheu WH,Lee WJ,et al. Levels of serum high mobility group box 1 were independently associated with cardiovascular risk in patients undergoing coronary angiography[J]. Clin Chim Acta,2018,483:130 4 34.
[34] Yao HC,Zhao AP,Han QF,et al. Correlation between serum highmobility group box4 levels and high-sensitivity C-reactive protein and troponin I in patients with coronary artery disease[J]. Exp Ther Med,2013,6(1):121424.
[35] Huang YY, Su W, Zhu ZW, et al. Elevated serum HMGB1 in pulmonary arterial hypertension secondary to congenital heart disease[J]. Vascul Pharmacol,2016,85:66-72.
[36] Andrassy M,Volz HC,Maack B,et al. HMGB1 is associated with atherosclerotic plaque composition and burden in patients with stable coronary artery disease[J]. PLoS One,2012,7(12):e52081.
[37] Karuppagounder V, Giridharan VV, Arumugam S,et al. Modulation of macrophage polarization and HMGB1-TLR2/TLR4 cascade plays a crucial role for cardiac remodeling in senescence-accelerated prone mice[J]. PLoS One,2016,11(4):e0152922.
[38] Wu RN, Yu TY, Zhou JC, et al. Targeting HMGB1 ameliorates cardiac fibrosis through restoring TLR2-mediated autophagy suppression in myocardial fibroblasts[J]. Int J Cardiol, 2018, 267:156-162.
[39] Ahrens I, Chen YC, Topcic D, et al. HMGB1 binds to activated platelets via the receptor for advanced glycation end products and is present in platelet rich human coronary artery thrombi[J].Thromb Haemost,2015,114(5):994-4003.
[40] Dozio E,Vianello E,Briganti S,et al. Expression of the receptor for advanced glycation end products in epicardial fat:Link with tissue thickness and local insulin resistance in coronary artery disease[J]. J Diabetes Res,2016,2016:2327341.
[41] Li Q,Li ZM,Sun SY,et al. PARP1 interacts with HMGB1 and promotes its nuclearexport in pathological myocardial hypertrophy[J/OL]. Acta Pharmacol Sin, 2018[2018-08-21]. https://www. nature. com/articles/s41401-018-0044-4.[publised online ahead of print July 20,2018].
[42] Yang J,Chen L, Yang J,et al. High mobility group box-4 induces migration of vascular smooth muscle cells via TLR4-dependent PI3K/Akt pathway activation[J]. Mol Biol Rep,2012,39(3):3361-3367.
[43] He YY, Wen Y, Zheng XN, et al. Intramyocardial delivery of HMGB1 by a novel thermosensitive hydrogel attenuates cardiac remodeling and improves cardiac functionafter myocardial infarction[J]. Cardiovasc Pharmacol,2013,61(4):283-290.
[44] Le K,Mo S,Lu X,et al. Association of circulating blood HMGB1levels with ischemic stroke:A systematic review and meta-analysis[J]. Neurol Res,2018,17:140.
[45]奥婷,张芹,肖淑英,许娜,等.HMGB1与缺血性脑卒中关系的研究进展[J].医学综述,2018,24(9):1681-1686.
[46] Richard SA,Sackey M,Su Z,et al. Pivotal neuroinflammatory and therapeutic role of high mobility group box 1 in ischemic stroke[J]. Biosci Rep,2017,37(6). pii:BSR20171104.
[47] Tian X,Liu C,Shu Z, et al. Review:Therapeutic targeting of HMGBI in stroke[J]. Curr Drug Deliv,2017,14(6):785-790.
[48] Shichita T, Hasegawa E, Kimura A,et al. Peroxiredoxin family proteins are key initiators of post-ischemic inflammation in the brain[J]. Nat Med,2012,18(6):911-917.
[49] Ooboshi H, Shichita T. DAMPs(damage-associated molecular patterns)and inflammation[J]. Nihon Rinsho, 2016,74(4):573-578.
[50] Zhang H, Xiong X, Liu J, et al. Emulsified isoflurane protects against transient focal cerebral ischemia injury in rats via the PI3K/Akt signaling pathway[J]. Anesth Analg,2016, 122(5):1377-1384.
[51] Choi JY,Kim BG. Toll-like receptor 2:A novel therapeutic target for ischemic white matter injury and oligodendrocyte death[J].Exp Neurobiol,2017,26(4):186494.
[52] Liu Y,Gao Y,Yang J,et al. MicroRNA-381 reduces inflammation and infiltration of macrophages in polymyositis via downregulating HMGB1[J]. Int J Oncol,2018,53(3):1332-1342.
[53] Zhan LY, Lei SQ, Zhaing BH, et al. Overexpression of miR-381relieves neuropathicpain development via targeting HMGB1 and CXCR4[J]. Biomed Pharmacother,2018,107:818-823.
[54] Hu J,Liu B, Zhao Q, et al. Bone marrow stromal cells inhibits HMGB1-mediated inflammation after stroke in type 2 diabetic rats[J]. Neuroscience,2016,324:11-19.
[55] Nakamura Y,Nakano T,Irie K,et al. Recombinant human soluble thrombomodulin ameliorates cerebral ischemic injury through a high-mobility group box 1 inhibitory mechanism without hemorrhagic complications in mice[J]. J Neurol Sci,2016,362:278-282.
[56] Ay L, Nasser R, Simon B, et al. Transcutaneous cervical vagus nerve stimulation ameliorates acute ischemic injury in rats[J].Brain Stimul,2016,9(2):166-473.
[57] Zhou S,Lu H,Chen R,et al. Angiotensin II enhances the acetylation and release of HMGB1 in RAW264. 7 macrophage[J/OL]. Cell Biol Int,2018[2018-08-17]. https://onlinelibrary.wiley. com/doi/abs/10. 1002/cbin.10984.[publised online ahead of print May 9,2018].
[58] Masson GS,Nair AR, Silva Soares PP,et al. Aerobic training normalizes autonomic dysfunction, HMGB1 content, microglia activation and inflammation in hypothalamic paraventricular nucleus of SHR[J]. Am J Physiol Heart Circ Physiol, 2015, 309(7):H1115-1122.