摘要
自身免疫性疾病(AID)是一类由自身抗原引起自身组织损伤的疾病。目前治疗AID仍以对症治疗和控制病情进展的药物为主,缺乏有效治疗措施,从而造成其致死率较高、治愈率较低的现状。因此对AID发病机制的详细阐明,在AID患者的临床及预后中都至关重要。许多研究表明缺氧诱导因子-1(HIF-1)参与AID的发病过程,本文将近年来关于HIF-1相关的信号通路及其在AID中作用的研究进展作一综述,以期为AID的临床治疗提供依据。
Autoimmune disease( AID) is a type of disease with self tissue damage caused by autoantigens. At present,the treatment of AID is still based on symptomatic treatment and drug control,and lacks effective treatment measures,resulting in a high mortality rate and a low cure rate. Therefore,the detailed elucidation of the pathogenesis of AID is crucial in the clinical and prognosis of patients with AID. Many studies have shown that hypoxia inducible factor-1( HIF-1) is involved in the pathogenesis of AID. This paper reviews recent advances in HIF-1 related signaling pathways and their role in AID,in order to provide a basis for clinical treatment of AID.
引文
[1]Semenza GL,Wang GL.A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation[J].Mol Cell Biol,1992,12(12):5447-5454.
[2]Semenza GL,Agani F,Booth G,et al.Structural and functional analysis of hypoxia-inducible factor 1[J].Kidney Int,1997,51(2):553-555.
[3]杨军,胡新华,张强,等.缺氧诱导因子1α及其相关基因在腹主动脉瘤中的表达[J].中国动脉硬化杂志,2004,12(5):507-510.Yang J,Hu XH,Zhang Q,et al.Expression of hypoxia-inducible factor 1αand its related genes in abdominal aortic aneurysm[J].Chin J Arterioscler,2004,12(5):507-510.
[4]Semenza GL.A compendium of proteins that interact with HIF-1α[J].Exp Cell Res,2017,356(2):128-135.
[5]Berra E,Roux D,Richard DE,et al.Hypoxia-inducible factor-1α(HIF-1α)escapes O2-driven proteasomal degradation irrespective of its subcellular localization:nucleus or cytoplasm[J].EMBORep,2001,2(7):615-620.
[6]李昭,王学彬.缺氧诱导因子-1α在风湿性疾病中的研究进展[J].中华风湿病学杂志,2018,22(1):54-57.Li Z,Wang XB.Research progress of hypoxia-inducible factor-1αin rheumatic diseases[J].Chin J Rheumatol,2018,22(1):54-57.
[7]Wu D,Potluri N,Lu J,et al.Structural integration in hypoxia-inducible factors[J].Nature,2015,524(7565):303-308.
[8]Semenza GL.Oxygen sensing,hypoxia-inducible factors,and disease pathophysiology[J].Ann Rev Pathol,2014,9:47-71.
[9]Mc Garry T,Biniecka M,Veale DJ,et al.Hypoxia,oxidative stress and inflammation[J].Free Radic Biol Med,2018,125:15-24.
[10]Hirai K,Furusho H,Hirota K,et al.Activation of hypoxiainducible factor 1 attenuates periapical inflammation and bone loss[J].Int J Oral Sci,2018,10(2):12.
[11]Koshikawa N,Hayashi J-I,Nakagawara A,et al.Reactive oxygen species-generating mitochondrial DNA mutation up-regulates hypoxia-inducible factor-1αgene transcription via phosphatidylinositol 3-kinase-Akt/protein kinase C/histone deacetylase pathway[J].J Biol Chem,2009,284(48):33185-33194.
[12]Chen J,Bai M,Ning C,et al.Gankyrin facilitates folliclestimulating hormone-driven ovarian cancer cell proliferation through the PI3K/AKT/HIF-1α/cyclin D1 pathway[J].Oncogene,2016,35(19):2506-2517.
[13]Zeng L,Zhou HY,Tang NN,et al.Wortmannin influences hypoxia-inducible factor-1 alpha expression and glycolysis in esophageal carcinoma cells[J].World J Gastroenterol,2016,22(20):4868-4880.
[14]Gao N,Shen L,Zhang Z,et al.Arsenite induces HIF-1αand VEGF through PI3K,Akt and reactive oxygen species in DU145human prostate carcinoma cells[J].Mol Cell Biochem,2004,255(1-2):33-45.
[15]Lei Q,Tan J,Yi S,et al.Mitochonic acid 5 activates the MAPK-ERK-yap signaling pathways to protect mouse microglial BV-2cells against TNFα-induced apoptosis via increased Bnip3-related mitophagy[J].Cell Mol Biol Lett,2018,23:14.
[16]Huang CY,Hsieh YL,Ju DT,et al.Attenuation of magnesium sulfate on CoCl2-induced cell death by activating ERK1/2/MAPKand inhibiting HIF-1αvia mitochondrial apoptotic signaling suppression in a neuronal cell line[J].Chin J Physiol,2015,58(4):244-253.
[17]Shi YH,Wang YX,Bingle L,et al.In vitro study of HIF-1 activation and VEGF release by b FGF in the T47D breast cancer cell line under normoxic conditions:involvement of PI-3K/Akt and MEK1/ERK pathways[J].J Pathol,2005,205(4):530-536.
[18]Sang N,Stiehl DP,Bohensky J,et al.MAPK signaling upregulates the activity of hypoxia-inducible factors by its effects on p300[J].J Biol Chem,2003,278(16):14013-14019.
[19]Lei Q,Qiang F,Chao D,et al.Amelioration of hypoxia and LPS-induced intestinal epithelial barrier dysfunction by emodin through the suppression of the NF-κB and HIF-1αsignaling pathways[J].Int J Mol Med,2014,34(6):1629-1639.
[20]Jiang H,Zhu Y,Xu H,et al.Activation of hypoxia-indecible factor-1 alpha via nuclear factor-kappa B in rat with chronic obstructive pulmonany disease[J].Acta Biochim Biophys Sin(Shanghai),2010,42(7):483-488.
[21]Semenza GL.Hypoxia-inducible factor 1(HIF-1)pathway[J].Sci Stke,2007,2007(407):cm8.
[22]Liu YV,Semenza GL.RACK1 vs.HSP90:competition for HIF-1αdegradation vs.stabilization[J].Cell Cycle,2007,6(6):656-659.
[23]Adhikary S,Eilers M.Transcriptional regulation and transformation by Myc proteins[J].Nat Rev Mol Cell Biol,2005,6(8):635-645.
[24]Diez H,Fischer A,Winkler A,et al.Hypoxia-mediated activation of Dll4-Notch-Hey2 signaling in endothelial progenitor cells and adoption of arterial cell fate[J].Exp Cell Res,2007,313(1):1-9.
[25]Shi Q,Li KJ,Treuer T,et al.Estimating the response and economic burden of rheumatoid arthritis patients treated with biologic disease-modifying antirheumatic drugs in Taiwan using the National Health Insurance Research Database(NHIRD)[J].PLoS One,2018,13(4):e0193489.
[26]Hu F,Liu H,Xu L,et al.Hypoxia-inducible factor-1αperpetuates synovial fibroblast interactions with T cells and B cells in rheumatoid arthritis[J].Eur J Immunol,2016,46(3):742-751.
[27]Hu F,Mu R,Zhu J,et al.Hypoxia and hypoxia-inducible factor-1αprovoke Toll-like receptor signalling-induced inflammation in rheumatoid arthritis[J].Ann Rheum Dis,2014,73(5):928-936.
[28]Hu F,Shi L,Mu R,et al.Hypoxia-inducible factor-1αand interleukin 33 form a regulatory circuit to perpetuate the inflammation in rheumatoid arthritis[J].PLoS One,2013,8(8):e72650.
[29]Rivas-Larrauri F,Yamazaki-Nakashimada MA.Systemic lupus erythematosus:Is it one disease?[J].Reumatol Clin,2016,12(5):274-281.
[30]Elshikha AS,Lu Y,Chen MJ,et al.Alpha 1 antitrypsin inhibits dendritic cell activation and attenuates nephritis in a mouse model of lupus[J].PLoS One,2016,11(5):e0156583.
[31]Feng CC,Ye QL,Zhu Y,et al.Lack of association between the polymorphisms of hypoxia-inducible factor 1A(HIF1A)gene and SLE susceptibility in a Chinese population[J].Immunogenetics,2014,66(1):9-13.
[32]Feng AP,Zhang Q,Li M,et al.High SIPA-1 expression in proximal tubules of human kidneys under pathological conditions[J].J Huazhong Univ Sci Technol Med Sci,2015,35(1):64-70.
[33]Huang Q,Chen SS,Li J,et al.miR-210 expression in PBMCs from patients with systemic lupus erythematosus and rheumatoid arthritis[J].Ir J Med Sci,2018,187(1):243-249.
[34]谭立明,冯晓晶,焦安君,等.强直性脊柱炎患者检测骨代谢指标潜在的临床价值[J].中国免疫学杂志,2017,33(10):1543-1546,1562.Tan LM,Feng XJ,Jiao AJ,et al.Potential clinical value of detecting bone metabolism markers in patients with ankylosing spondylitis[J].Chin J Immunol,2017,33(10):1543-1546,1562.
[35]ProcházkováL,Cervenák V,Soucek M.Axial spondyloarthritis[J].Vnitr Lek,2018,64(2):108-116.
[36]Masuda K,Tanabe K,Ujike H,et al.Deletion of pro-angiogenic factor vasohibin-2 ameliorates glomerular alterations in a mouse diabetic nephropathy model[J].PLoS One,2018,13(4):e0195779.
[37]Wang JC,Li XX,Sun X,et al.Activation of AMPK by simvastatin inhibited breast tumor angiogenesis via impeding HIF-1α-induced pro-angiogenic factor[J].Cancer Sci,2018,109(5):1627-1637.
[38]Hussain MS,Tripathi V.Smoking under hypoxic conditions:a potent environmental risk factor for inflammatory and autoimmune diseases[J].Mil Med Res,2018,5(1):11.
[39]Lv XM,Li MD,Cheng S,et al.Neotuberostemonine inhibits the differentiation of lung fibroblasts into myofibroblasts in mice by regulating HIF-1αsignaling[J].Acta Pharmacol Sin,2018,39(9):1501-1512.