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Omentin-1 attenuates adipose tissue inflammation via restoration of txnip/NLRP3 signaling in high-fat diet-induced obese mice

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FUNDAMENTAL & CLINICAL PHARMACOLOGY 2020年第6期34卷 721-735页

作者： Zhou, Hongli Zhang, Zuo Qian, Guisheng Zhou, Jiyin Army Med Univ Affiliated Hosp 2 Natl Drug Clin Trial Inst Chongqing 400037 Peoples R China Army Med Univ Affiliated Hosp 2 Inst Resp Dis Chongqing 400037 Peoples R China

Omentin-1 is an adipokine expressed by the adipose tissue and is reduced in obesity. This study was designed to calculate the protective efficiency and mechanism of omentin-1 against inflammation of the adipose tissue in obese mice. A transgenic mouse model with omentin-1 protein overexpression was established by crossing omentin-1 transgenic mice with Fabp4-Cre mice. Obesity was induced in the mice by feeding them a high-fat diet for 10 weeks. Fabp4-Cre-mediated overexpression of omentin-1 significantly increased serum omentin-1 level, serum anti-inflammatory factor levels, and expression of M2-specific mRNAs;inhibited body weight and adipose tissue weight gain;improved glucose tolerance, insulin tolerance, and insulin sensitivity;decreased serum levels of insulin and proinflammatory factors, adipocyte size, and expression of M1-specific mRNAs;suppressed macrophage infiltration;downregulated expression of proinflammatory factors;upregulated expression of anti-inflammatory factors;and inhibited thioredoxin-interacting protein (txnip)/NOD-like receptor 3 (NLRP3) signaling in the adipose tissue of obese mice. An NLRP3 inhibitor (20 mg/kg MCC950) exhibited the same effects as overexpression of omentin-1. Pretreatment with omentin-1 inhibited lipopolysaccharide-induced inflammation via txnip/NLRP3 signaling in RAW 264.7 macrophages. These findings suggest that omentin-1 suppresses adipose tissue inflammation in obese mice, at least partly, via inhibiting the txnip/NLRP3 signaling pathway.

关键词： adipose tissue inflammation obese mice Omentin-1 overexpression txnip NLRP3 signaling pathway

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Rapid and persistent loss of txnip in HT22 neuronal cells under carbonyl and hyperosmotic stress

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NEUROCHEMISTRY INTERNATIONAL 2020年 132卷 104585页

作者： Dafre, Alcir Luiz Schmitz, Ariana Ern Maher, Pamela Univ Fed Santa Catarina Biochem Dept BR-88040900 Florianopolis SC Brazil Salk Inst Biol Studies Cellular Neurobiol Lab 10010 N Torrey Pines Rd La Jolla CA 92037 USA Catolica Joinville Ctr Univ BR-89203005 Joinville SC Brazil

Thioredoxin interacting protein (txnip) binds to thioredoxin thereby limiting its activity, but it also promotes internalization of glucose transporters, participates in inflammasome activation, and controls autophagy. Published data and this work demonstrate that txnip responds to a number of apparently unrelated stresses, such as serum deprivation, pH change, and oxidative, osmotic and carbonyl stress. Interestingly, we noticed that hyperosmotic (NaCl) and carbonyl (methylglyoxal, MGO) stresses in HT22 neuronal cells produced a rapid loss of txnip (half-life similar to 12 min), prompting us to search for possible mechanisms controlling this txnip loss, including pH change, serum deprivation, calcium metabolism and inhibition of the proteasome and other proteases, autophagy and MAPKs. None of these routes stopped the txnip loss induced by hyperosmotic and carbonyl stress. Besides transcriptional, translational and microRNA regulation, there is evidence indicating that mTOR and AMPK also control txnip expression. Indeed, AMPK-deficient mouse embryonic fibroblasts failed to respond to phenformin (AMPK activator) and compound C (AMPK inhibitor), while rapamycin induced a marked increase in txnip levels, confirming the known AMPK/mTOR control over txnip. However, the txnip loss induced by NaCl or MGO were observed even in AMPK deficient MEFs or after mTOR inhibition, indicating AMPK/mTOR does not participate in this rapid txnip loss. These results suggest that rapid txnip loss is a general and immediate response to stress that can improve energy availability and antioxidant protection, eventually culminating in better cell survival.

关键词： txnip VDUP2 Hyperosmotic stress Carbonyl stress AMPK Stress resistance

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Endoplasmic reticulum stress may activate NLRP3 inflammasomes via txnip in preeclampsia

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CELL AND TISSUE RESEARCH 2020年第3期379卷 589-599页

作者： Yang, Yong Li, Jianxin Han, Ting-Li Zhou, Xiaobo Qi, Hongbo Baker, Philip N. Zhou, Wei Zhang, Hua Chngqing Hlth Ctr Women & Children Dept Obstet 120 Longshan Rd Chongqing 400021 Peoples R China Chongqing Med Univ Affiliated Hosp 1 Dept Obstet & Gynecol 1 Youyi Rd Chongqing 400016 Peoples R China Chongqing Med Univ Canada China New Zealand Joint Lab Maternal & Fet 1 Yixueyuan Rd Chongqing 400016 Peoples R China Univ Leicester Coll Med Biol Sci & Psychol POB 138 Leicester LE1 9HN Leics England

Preeclampsia (PE) development is often associated with placental immune and inflammatory dysregulation, as well as endoplasmic reticulum (ER) stress. However, the mechanisms linking ER stress and inflammatory dysregulation to PE have not been elucidated. It has been reported that thioredoxin-interacting protein (txnip), which can bind with and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome, is a key point in immune regulation. Recent experimental evidence suggests that activated NLRP3 inflammasomes can activate interleukin-1 beta (IL-1 beta) production in the placenta of patients with PE. The objective of the current study was to explore if txnip plays a critical signaling role linking ER stress with NLRP3 inflammasome activation in PE. We hypothesized that ER stress would induce txnip production, which would bind with NLRP3 inflammasomes to activate IL-1 beta production. These cells showed a higher protein level of NLRP3 and IL-1 beta, as well as a higher enzymatic activity of caspase-1, indicating enhanced inflammatory dysregulation and ER stress. Cells transfected with txnip siRNA showed reduced NLRP3 inflammasome activation. Cells treated with 4-phenylbutyric acid, an inhibitor of ER stress, showed a similar result. Outgrowth of the explant with txnip lentivirus in H/R or tunicamycin (inducers of ER stress) was also measured to verify our hypothesis. These findings demonstrated that txnip could influence inflammatory dysregulation by mediating ER stress and NLRP3 inflammasome activation in PE. This novel mechanism may further explain the inflammation observed at the maternal-fetal interface, which leads to placental dysfunction in a patient with PE.

关键词： Preeclampsia (PE) Inflammation Endoplasmic reticulum (ER) stress NLRP3 txnip

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BRAFi induced demethylation of miR-152-5p regulates phenotype switching by targeting txnip in cutaneous melanoma

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APOPTOSIS 2020年第3-4期25卷 179-191页

作者： Li, Kezhu Tang, Mingrui Tong, Shuang Wang, Chenchao Sun, Qiang Lv, Mengzhu Sun, Xu Wang, Ting Jin, Shifeng China Med Univ Affiliated Hosp 1 Dept Plast Surg 155 Nanjing North St Shenyang 110001 Liaoning Peoples R China

Treatment of advanced BRAF(V600)-mutant melanoma using BRAF inhibitors (BRAFi) eventually leads to drug resistance and selects for highly metastatic tumor cells. We compared the most differentially dysregulated miRNA expression profiles of vemurafenib-resistant and highly-metastatic melanoma cell lines obtained from GEO DataSets. We discovered miR-152-5p was a potential regulator mediating melanoma drug resistance and metastasis. Functionally, knockdown of miR-152-5p significantly compromised the metastatic ability of BRAFi-resistant melanoma cells and overexpression of miR-152-5p promoted the formation of slow-cycling phenotype. Furthermore, we explored the cause of how and why miR-152-5p affected metastasis in depth. Mechanistically, miR-152-5p targeted txnip which affected metastasis and BRAFi altered the methylation status of MIR152 promoter. Our study highlights the crucial role of miR-152-5p on melanoma metastasis after BRAFi treatment and holds significant implying that discontinuous dosing strategy may improve the benefit of advanced BRAF(V600)-mutant melanoma patients.

关键词： miR-152-5p Melanoma Metastasis BRAFi txnip

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MiRNA-338-5p reduced inflammation through txnip/NLRP3 inflammasome axis by CXCR4 in DSS-induced colitis

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MOLECULAR & CELLULAR TOXICOLOGY 2020年第2期16卷 149-158页

作者： Huang, Xunru Lin, Yijuan Zheng, Xueyan Wang, Chengdang Fujian Med Univ Affiliated Hosp 1 Dept Gastroenterol 20 Cha Zhong Rd Fuzhou 350004 Fujian Peoples R China Fujian Med Univ Digest Dis Lab Fuzhou 350004 Fujian Peoples R China

Backgrounds miRNAs, about 20-25 bases in length, are short-chain non-coding RNAs existing in the body, which are widely involved in the biological regulation of the organism. miRNAs inhibit the expression of target genes by specifically binding to target genes, thereby exerting biological effects. Methods We investigated the function of miRNA-338-5p on inflammation and its possible mechanisms in colitis Results In DSS-induced colitis model, we found that miRNA-338-5p expression was reduced. Therefore, down-regulation of miRNA-338-5p increased inflammation and induced CXCR4, txnip, and NLRP3 protein expression in in vitro model. Meanwhile, over-expression of miRNA-338-5p reduced inflammation and suppressed CXCR4, txnip, and NLRP3 protein expression in in vitro model. Therefore, miRNA-338-5p may possess anti-inflammatory effects in colitis. However, si-CXCR4 reduced the anti-inflammatory effects of miRNA-338-5p in invitro model. Then, si-NLRP3 also reduced the anti-inflammatory effects of miRNA-338-5p in in vitro model. These results showed that miRNA-338-5p reduced inflammation in colitis through the txnip/NLRP3 inflammasome axis by CXCR4. Conclusion MiRNA-338-5p may potentially serve as novel therapeutic avenues for colitis.

关键词： miRNA-338-5p txnip NLRP3 CXCR4 Colitis

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Inhibition of EZH2 attenuates coronary heart disease by interacting with microRNA-22 to regulate the txnip/nuclear factor-κB pathway

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EXPERIMENTAL PHYSIOLOGY 2020年第12期105卷 2038-2050页

作者： Liu, Yong Dai, Chuanzhong Lei, Yuping Wu, Wenzhen Liu, Wen Liaocheng Peoples Hosp Dept Cardiol 67 Dongchang West Rd Liaocheng 252000 Shandong Peoples R China

New Findings What is the central question of this study? The relevance of microRNA-22 (miR-22) has been indicated in coronary heart disease (CHD). How does it exert a protective role in CHD? What is the main finding and its importance? EZH2 inhibited transcription of the miR-22 promoter, thus modulating cell proliferation in human umbilical vein endothelial cells and vascular smooth muscle cells to induce CHD. MicroRNA-22 (miR-22) was indicated to modulate cell proliferation in human umbilical vein endothelial cells (HUVECs) under exposure to environmental toxicants. In the present study, we investigated the involvement of miR-22 in the mediation of HUVEC and vascular smooth muscle cell (VSMC) function, hence in the development of coronary heart disease (CHD). miR-22 expression was reduced in serum of CHD patients. Restoration of miR-22 decreased the proliferation, migration and invasion of VSMCs and increased apoptotic cells and inflammatory factors. In contrast, upregulation of miR-22 led to opposite trends in HUVECs. Chromatin immunoprecipitation and dual-luciferase assays validated that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibited transcription of miR-22 promoter. EZH2, overexpressed in serum from CHD patients, diminished VSMC apoptosis, but facilitated HUVEC apoptosis. Luciferase reporter assays confirmed that thioredoxin-interacting protein (txnip) was a new direct target of miR-22. Overexpression of txnip blocked the function of miR-22 in HUVECs and VSMCs. Taken together, these findings will shed light on the role and mechanism of EZH2 in viability, migration, invasion and apoptosis via the miR-22/txnip axis in VSMCs and HUVECs, which might provide new insights into the treatment of CHD.

关键词： coronary heart disease EZH2 microRNA‐ 22 nuclear factor‐ κ B txnip

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鄂尔多斯细毛羊LMNB1基因和txnip基因多态性与羊毛性状关联分析

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家畜生态学报 2022年第10期43卷 23-29页

作者：付雪峰谷英吴翠玲德德玛孟根曹斯庆毕力格斯登丹巴田可川新疆畜牧科学院畜牧研究所新疆绒毛用羊遗传育种与繁殖实验室(XJYS1105)新疆乌鲁木齐830011 鄂尔多斯市农牧业科学研究院内蒙古鄂尔多斯017100 新疆师范大学生命科学学院中亚区域跨境有害生物联合控制国际研究中心/新疆特殊环境物种多样性应用与调控实验室新疆乌鲁木齐830017 内蒙古鄂尔多斯市乌审旗家畜改良工作站内蒙古鄂尔多斯017300 山东省农业科学院畜牧兽医研究所山东济南250100

该研究旨在寻找细毛羊主要经济性状的分子标记。以462只周岁鄂尔多斯细毛羊母羊为试验动物,联合DNA混池和Snapshot技术,检测LMNB1基因和txnip基因多态性,采用SAS9.2对LMNB1基因和txnip基因突变位点与羊毛性状进行关联分析。结果表明:鄂... 详细信息

该研究旨在寻找细毛羊主要经济性状的分子标记。以462只周岁鄂尔多斯细毛羊母羊为试验动物,联合DNA混池和Snapshot技术,检测LMNB1基因和txnip基因多态性,采用SAS9.2对LMNB1基因和txnip基因突变位点与羊毛性状进行关联分析。结果表明:鄂尔多斯细毛羊的LMNB1基因有1个Indel(Indel1)、4个SNP同义突变(SNP1、SNP2、SNP3、SNP4);txnip基因在3'UTR区有1个突变(SNP5)。LMNB1基因Indel1-SNP1突变位点ATCT基因型和TTTT基因型群体纤维直径变异系数显著高于AACC基因型(P<0.05),ATCT基因型和TTTT基因型之间差异不显著(P>0.05);txnip基因SNP5突变位点TT基因型平均纤维直径显著高于CT基因型(P<0.05),极显著高于CC基因型(P<0.01);CC基因型和CT基因型之间平均纤维直径差异不显著(P>0.05)。结果提示,txnip基因SNP5可作为影响鄂尔多斯细毛羊绒毛纤维直径的分子标记,为鄂尔多斯细毛羊超细型群体的选育提供试验依据。

关键词：鄂尔多斯细毛羊羊毛性状 LMNB1 txnip 多态性

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Oridonin attenuates carrageenan-induced pleurisy via activation of the KEAP-1/Nrf2 pathway and inhibition of the txnip/NLRP3 and NF-κB pathway in mice

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INFLAMMOPHARMACOLOGY 2020年第2期28卷 513-523页

作者： Yang, Huahong Huang, Jingbo Gao, Yanli Wen, Zhongmei Peng, Liping Ci, Xinxin Jilin Univ Hosp 1 Inst Translat Med Changchun Peoples R China Jilin Univ Hosp 1 Dept Resp Med Changchun Peoples R China Jilin Univ Hosp 1 Dept Pediat Ultrasound Changchun 130061 Peoples R China

The classic NLRP3 inflammasome and NF-kappa B molecular pathways are activated in many inflammatory-related diseases, such as pleurisy. Because oridonin (Ori) has been indicated as a covalent NLRP3 inhibitor with strong anti-inflammasome activity, we herein aimed to assess the effects of Ori in a mouse model of carrageenan (CAR)-induced pleurisy. The results showed that CAR caused hemorrhaging and exudation of lung tissues and the release of inflammatory factors (TNF-alpha, IL-6 and IL-1 beta), effects that were significantly reduced by treatment with Ori. In addition, increased neutrophil infiltration, protein concentrations and volumes were found in the exudates of the CAR group, and these phenomena were suppressed by Ori treatment. Regarding cellular pathways, Ori could alleviate the CAR-activated NF-kappa B and txnip/NLRP3 pathways. Additionally, oxidative stress was shown to be involved in the pathogenesis of pleurisy, but possible mechanisms remain to be explored. Herein, Ori reversed the CAR-induced depletion of GSH and SOD and the CAR-induced increases in ROS, MPO and MDA levels. Furthermore, Ori inhibited NOX-4 levels, initiated the dissociation of KEAP-1 from Nrf2, activated the downstream genes HO-1 and exerted antioxidative effects on CAR-induced pleurisy. In conclusion, Ori conferred protection against CAR-induced pleurisy via Nrf2-dependent antioxidative and NLRP3-dependent anti-inflammatory properties.

关键词： Oridonin Carrageenan Pleurisy KEAP-1 Nrf2 Nf-kappa b txnip NLRP3

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Targeting endothelial thioredoxin-interacting protein (txnip) protects from metabolic disorder-related impairment of vascular function and post-ischemic revascularisation

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ANGIOGENESIS 2020年第2期23卷 249-264页

作者： Domingues, Alison Boisson-Vidal, Catherine Marquet de Rouge, Perrine Dizier, Blandine Sadoine, Jeremy Mignon, Virginie Vessieres, Emilie Henrion, Daniel Escriou, Virginie Bigey, Pascal Chaussain, Catherine Smadja, David M. Nivet-Antoine, Valerie Univ Paris Fac Pharm INSERM 1140 Innovat Therapies Haemostasis F-75006 Paris France Univ Paris Dent Sch Lab Orofacial Pathol Imaging & Biotherapies EA 2496 F-92120 Montrouge France Univ Paris CNRS INSERM 3612 PTICM F-75006 Paris France Univ Angers CNRS INSERM 1083 MITOVASC F-49045 Angers France Univ Paris Chim ParisTech CNRS UMR 8258INSERM 1022UTCBS F-75006 Paris France Bretonneau Hosp AP HP Odontol Dept F-75018 Paris France Georges Pompidou European Hosp AP HP Serv Hematol F-75015 Paris France Georges Pompidou European Hosp AP HP Fdn Carpentier Lab Rech Biochirug F-75015 Paris France Hop Necker Enfants Malad AP HP Clin Biochem Dept F-75015 Paris France

Introduction Although thioredoxin-interacting protein (txnip) is involved in a variety of biological functions, the contribution of endothelial txnip has not been well-defined in regards to endothelial and vascular function or in post-ischemic revascularisation. We postulated that inhibition of endothelial txnip with siRNA or in a Cre-LoxP system could be involved in protection from high fat, high protein, low carbohydrate (HFHPLC) diet-induced oxidative stress and endothelial dysfunction, leading to vascular damage and impaired revascularisation in vivo. Methods and results To investigate the role of endothelial txnip, the txnip gene was deleted in endothelial cells using anti-txnip siRNA treatment or the Cre-LoxP system. Murine models were fed a HFHPLC diet, known to induce metabolic disorders. Endothelial txnip targeting resulted in protection against metabolic disorder-related endothelial oxidative stress and endothelial dysfunction. This protective effect mitigates media cell loss induced by metabolic disorders and hampered metabolic disorder-related vascular dysfunction assessed by aortic reactivity and distensibility. In aortic ring cultures, metabolic disorders impaired vessel sprouting and this alteration was alleviated by deletion of endothelial txnip. When subjected to ischemia, mice fed a HFHPLC diet exhibited defective post-ischemic angiogenesis and impaired blood flow recovery in hind limb ischemia. However, reducing endothelial txnip rescued metabolic disorder-related impairment of ischemia-induced revascularisation. Conclusion Collectively, these results show that targeting endothelial txnip in metabolic disorders is essential to maintaining endothelial function, vascular function and improving ischemia-induced revascularisation, making txnip a potential therapeutic target for therapy of vascular complications related to metabolic disorders.

关键词： txnip Metabolic disorders Endothelial dysfunction Oxidative stress Arterial damage Post-ischemic revascularisation

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WT1通过上调糖酵解关键基因txnip抑制肾癌细胞增殖的分子机制研究

WT1通过上调糖酵解关键基因TXNIP抑制肾癌细胞增殖的分子机制研究

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作者：秦翰成右江民族医学院

学位级别：硕士

目的:研究WT1通过调节txnip介导的糖酵解过程进而抑制肾癌细胞增殖的作用及相关分子机制。方法:（1）利用TIMER、UALCAN、HPA、Linked Omics以及DAVID等多种在线生物信息学工具,研究TCGA数据库中WT1基因在肾透明细胞癌（kidney renal cl... 详细信息

目的:研究WT1通过调节txnip介导的糖酵解过程进而抑制肾癌细胞增殖的作用及相关分子机制。方法:（1）利用TIMER、UALCAN、HPA、Linked Omics以及DAVID等多种在线生物信息学工具,研究TCGA数据库中WT1基因在肾透明细胞癌（kidney renal clear cell carcinoma,KIRC）组织和癌旁组织中的表达水平,并对WT1相关基因进行基因本体论（gene ontology,GO）和京都基因与基因组百科全书（kyoto encyclopedia of genes and genomes,KEGG）信号通路富集分析。（2）利用Co Cl2模拟缺氧环境,检测Co Cl2处理后HEK293细胞的葡萄糖摄取和乳酸合成的变化;RT-q PCR检测Co Cl2处理后HEK293细胞中WT1、MLXIP和txnip的表达水平。（3）使用葡萄糖（GLU）测试盒和乳酸（LD）测试盒对肾癌细胞A498过表达WT1后的葡萄糖摄取和乳酸合成的变化进行检测;利用RT-q PCR检测肾癌细胞A498过表达WT1后的表达水平。（4）通过生物发光成像系统检测细胞发光情况以确定过表达WT1是否抑制肾癌细胞增殖;通过流式分析检测过表达WT1对肾癌细胞A498细胞周期分布的影响;在裸鼠荷瘤模型中检测过表达WT1对肾癌细胞增殖的影响;通过免疫组化和RT-q PCR检测肿瘤组织中WT1的表达水平。（5）利用TIMER、UALCAN、HPA、Linked Omics和DAVID等在线生物信息学工具分析TCGA数据库中txnip基因在KIRC组织和癌旁组织中的表达水平,并对txnip相关基因进行GO和KEGG信号通路富集分析。（6）采用葡萄糖（GLU）测试盒和乳酸（LD）测试盒检测肾癌细胞A498过表达txnip后的葡萄糖摄取和乳酸合成的变化;利用RT-q PCR和Western Blot检测肾癌细胞A498过表达txnip后的m RNA和蛋白表达水平。（7）采用RT-q PCR技术和Western Blot检测肾癌细胞A498过表达WT1后MLXIP和txnip的表达水平,通过荧光素酶报告基因实验研究WT1对MLXIP启动子转录活性的影响。结果:（1）WT1低表达于肾透明细胞癌。GO分析显示,WT1与葡萄糖代谢途径（glucose metabolic process）、细胞葡萄糖稳态（cellular glucose homeostasis）及细胞增殖（cell proliferation）等生物学过程密切相关;KEGG分析表明,WT1参与了肾透明细胞癌（kidney renal clear cell carcinoma,KIRC）的PI3K-Akt信号通路（PI3K-Akt signaling pathway）、NF-κB信号通路（NF-kappa B signaling pathway）和p53信号通路（p53 signaling pathway）等。（2）Co Cl2处理后HEK293细胞葡萄糖摄取和乳酸合成增加,具有浓度梯度依赖性;同时WT1、MLXIP和txnip的m RNA表达水平下降。（3）过表达WT1抑制肾癌细胞葡萄糖摄取和乳酸合成。（4）过表达WT1可在体内及外条件下抑制肾癌细胞A498增殖;过表达WT1可以诱导肾癌细胞发生G2/M期阻滞。（5）txnip在肾透明细胞癌中表达较低;txnip表达水平与KIRC患者病理分级具有相关性,随着KIRC患者病理分级逐渐增加,txnip表达水平下降;txnip的表达水平与KIRC患者的总体生存率（overall survival,OS）显著相关,txnip高表达组患者的OS明显高于txnip低表达组患者。GO富集分析结果显示,txnip表达相关基因显著富集到葡萄糖代谢过程的调节（regulation of glucose metabolic process）、细胞迁移（cell migration）及细胞周期（cell cycle）等生物学过程;细胞组分富集分析结果显示txnip相关基因主要位于线粒体基质（mitochondrial matrix）、高尔基膜（golgi membrane）及核膜（nuclear membrane）等区域;分子功能富集分析结果显示,txnip表达相关基因与RNA聚合酶结合（RNA polymerase binding）、泛素结合（ubiquitin binding）及核糖体结合（ribosome binding）等显著相关。KEGG分析结果显示,txnip表达相关基因主要与HIF-1信号通路（HIF-1signaling pathway）、PI3K-Akt信号通路（PI3K-Akt signaling pathway）及AMPK信号

关键词： WT1 txnip 肾癌糖酵解细胞增殖

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