预约演示

更新于：2025-05-07

TXNIP

更新于：2025-05-07

基本信息

别名

ARRDC6、EST01027、HHCPA78

+ [7]

简介

May act as an oxidative stress mediator by inhibiting thioredoxin activity or by limiting its bioavailability (PubMed:17603038). Interacts with COPS5 and restores COPS5-induced suppression of CDKN1B stability, blocking the COPS5-mediated translocation of CDKN1B from the nucleus to the cytoplasm (By similarity). Functions as a transcriptional repressor, possibly by acting as a bridge molecule between transcription factors and corepressor complexes, and over-expression will induce G0/G1 cell cycle arrest (PubMed:12821938). Required for the maturation of natural killer cells (By similarity). Acts as a suppressor of tumor cell growth (PubMed:18541147). Inhibits the proteasomal degradation of DDIT4, and thereby contributes to the inhibition of the mammalian target of rapamycin complex 1 (mTORC1) (PubMed:21460850).

关联

项与 TXNIP 相关的药物

VCTX-211

靶点

B2M x HLA-E x MANF x PDL1 x TNFAIP3 x TXNIP

作用机制

B2M抑制剂 [+6]

在研机构

CRISPR Therapeutics AG

原研机构

ViaCyte, Inc. [+1]

在研适应症

1型糖尿病

非在研适应症-

最高研发阶段临床1/2期

首次获批国家/地区-

首次获批日期1800-01-20

TIX-100

靶点

TXNIP

作用机制

TXNIP inhibitors

在研机构

TIXiMED, Inc.

原研机构

TIXiMED, Inc.

在研适应症-

非在研适应症-

最高研发阶段临床1期

首次获批国家/地区-

首次获批日期1800-01-20

W2476

靶点

TXNIP

作用机制

TXNIP modulators

在研机构-

原研机构

中国科学院上海药物研究所

在研适应症-

非在研适应症

糖尿病

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

项与 TXNIP 相关的临床试验

NCT06800729

/ Recruiting临床1期

A Single Center, Single Dose, Randomized, Placebo-controlled Study to Evaluate Safety, Tolerability and Pharmacokinetics of Orally Administered TIX100 in Healthy Subjects

开始日期2025-01-01

申办/合作机构

TIXiMED, Inc.

NCT05565248

/ Recruiting临床1/2期

An Open-Label, First-in-Human Study Evaluating the Safety, Tolerability, and Efficacy of VCTX211 Combination Product in Subjects With Type 1 Diabetes Mellitus (T1D)

This is an open-label, multicenter, Phase 1/2 study evaluating the Safety, Tolerability, and Efficacy of VCTX211 Combination Product in Subjects with T1D

开始日期2023-01-20

申办/合作机构

CRISPR Therapeutics AG

[+1]

100 项与 TXNIP 相关的临床结果

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100 项与 TXNIP 相关的转化医学

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0 项与 TXNIP 相关的专利（医药）

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2,074

项与 TXNIP 相关的文献（医药）

2025-12-01·Molecular Biology Reports

High Glucose-induced transcriptomic changes in human trabecular meshwork cells

Article

作者: Singh, Shivendra ; Raghavan, Srimathi ; Soundararajan, Avinash ; Pattabiraman, Padmanabhan P ; Patel, Niketa A

AbstractGlaucoma is a leading cause of irreversible blindness, often associated with elevated intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction. Diabetes mellitus (DM) is recognized as a significant risk factor for glaucoma; however, the molecular mechanisms through which hyperglycemia affects TM function remain unclear. This study investigated the impact of high glucose on gene expression in human TM (HTM) cells to uncover pathways that contribute to TM dysfunction and glaucoma pathogenesis under diabetic conditions. Primary HTM cells were cultured under normoglycemic (5.5 mM) and hyperglycemic (30 mM) conditions for seven days, followed by mRNA sequencing (mRNA-seq) to identify differentially expressed genes, with quantitative PCR (qPCR) used for confirmatory analysis. STRING network analysis was performed to predict potential interactions among upregulated and downregulated genes. mRNA-seq analysis revealed 25 significantly differentially expressed genes in high glucose conditions, including upregulated genes associated with oxidative stress, apoptosis, autophagy, immune response, and fibrosis. Notably, TXNIP gene was significantly upregulated, indicating increased oxidative stress and apoptosis in TM cells, while downregulation of autophagy-related genes, such as HSPA6 and LAMP3, suggests compromised protein quality control. Immune response genes, including CCL7 and CHI3L1, were upregulated, suggesting an inflammatory response to oxidative stress. Increased expression of fibrosis-related genes, such as SNAI1, FGF7, and KRT19, and an increase in ECM proteins like Collagen 1 and FN accumulation and fibril formation suggest increased fibrosis of TM in diabetic conditions, potentially elevating IOP. Metabolic changes in diabetic patients could therefore lead to TM dysfunction, impair aqueous humor outflow, and elevate IOP, thereby increasing glaucoma risk. Targeting oxidative stress and fibrosis pathways offers therapeutic strategies to mitigate glaucoma progression in diabetic populations.

2025-06-01·Life Sciences

M2 macrophage derived exosomal miR-20a-5p ameliorates trophoblast pyroptosis and placental injuries in obstetric antiphospholipid syndrome via the TXNIP/NLRP3 axis

Article

作者: Zhang, Hongyuan ; Lv, Qingfeng ; Liu, Qian ; Huo, Ruiheng ; Wang, Xietong ; Jiang, Ning ; Li, Lei ; Jing, Die ; Dong, Tingting ; Chen, Pengzheng ; Xu, Mingyang

AIMObstetric antiphospholipid syndrome (OAPS) is a pregnancy-related complication characterized by trophoblast pyroptosis and placental injury induced by antiphospholipid antibodies (aPLs). M2-polarized macrophage-derived exosomes (M2-exos) exert anti-inflammatory, immunomodulatory, and growth-promoting effects in various autoimmune diseases and tumors. However, their role in OAPS is not yet clear. Therefore, in this study, we isolated M2-exos from M2 macrophages and investigated their effects on trophoblast proliferation, death, migration, invasion, and pyroptosis following stimulation using aPLs.MAIN METHODSFirst, we established an animal model of OAPS and thereafter treated the OAPS mice with exogenous M2-exos via injection through the tail vein. Then to clarify the roles of miR-20a-5p and thioredoxin-interacting protein (TXNIP) in OAPS, we performed gain- or loss-of-function assays, and used GraphPad Prism software to analyze the collected data with statistical significance set at P < 0.05.KEY FINDINGSMicroRNAs (miRNAs) sequencing revealed the enrichment of miR-20a-5p in M2-exos, and these M2-exos significantly alleviated aPLs-induced trophoblast dysfunction. Our results also indicated that M2-exos delivered miR-20a-5p to trophoblast cells directly targeted thioredoxin-interacting protein (TXNIP), and thus suppressed the TXNIP/NLRP3 pathway, reduced pyroptosis and inflammation in trophoblast cells, and improved placental function and fetal development.SIGNIFICANCEM2-exos improve pregnancy outcomes in OAPS via the miR-20a-5p/TXNIP/NLRP3 axis, and thus represent as a novel therapeutic approach for aPLs-induced OAPS.

2025-06-01·Toxicology Reports

Bacillus clausii spores maintain gut homeostasis in murine ulcerative colitis via modulating microbiota, apoptosis, and the TXNIP/NLRP3 inflammasome cascade

Article

作者: Hammam, Olfat A ; El-Lakkany, Naglaa M ; Seif El-Din, Sayed H ; Salem, Maha B

Ulcerative colitis (UC), a persistent immune-mediated disorder lacking effective treatment, is distinguished by gut microbiota dysbiosis, abnormal activation of the NLRP3 inflammasome pathway, and apoptosis. Despite growing attention to these factors, understanding their significance in UC pathogenesis remains a challenge. The present study explores the potential therapeutic impact of Bacillus clausii (Bc) spores in a murine UC model induced by drinking 4 % (w/v) dextran sulfate sodium (DSS) in C57BL/6 mice. Subsequently, the DSS-induced mice were orally administered either Bc at varying concentrations (10⁵ and 10¹⁰ Colony forming unit, CFU) or sulfasalazine (SSZ) at a dosage of 200 mg/kg for 7 days. The disease-specific activity index (DAI) was calculated daily utilizing parameters such as body weight, diarrhea, and bloody stool. Changes in fecal Firmicutes and Bacteroidetes abundance, colonic TXNIP and NLRP3 contents, as well as colonic caspase-1, IL-1β, Bax, and Bcl-2 expression, were investigated. Additionally, markers related to oxidative stress and inflammation, histopathological changes and caspase-3 immunohistochemistry testing were conducted. DSS-treated mice had significantly higher DAI scores compared to controls, indicating severe colitis. However, SSZ treatment or Bc (10⁵ CFU) dramatically lowered DAI scores, with the highest Bc dosage (10¹⁰ CFU) producing the greatest improvement. Furthermore, Bc (10¹⁰ CFU) substantially (p < 0.05) boosted fecal Firmicutes while decreased Bacteroidetes, indicating reversal of gut dysbiosis. Bc effectively reduced colonic oxidative stress and inflammation by replenishing GSH and catalase and modulating the NF-κB, Nrf2/HO-1, and TXNIP/NLRP3 pathways. Additionally, Bc (10¹⁰ CFU) exhibited histologically almost normal mucosa, with maintained architecture and reduced apoptosis, as seen by normalization of Bcl2 and Bax with decreased caspase-3. Collectively, these findings point to the potential usefulness of Bc spores in preventing and treating DSS-induced colitis, positioning them as a promising candidate for UC management.

项与 TXNIP 相关的新闻（医药）

2024-12-19

·Business Wire

TIXiMED Announces a $2.65M Program-Related Investment from the Helmsley Charitable Trust to Initiate Clinical Trials of Its Novel Oral Therapy for Beta Cell Survival and Function

BIRMINGHAM, Ala.--( BUSINESS WIRE )-- TIXiMED, Inc. ( https://tiximed.com ), a clinical-stage pharmaceutical company based on the breakthrough discovery that TXNIP plays an important role in the development and progression of diabetes, has secured a program-related investment in the form of a $2.65M loan from The Leona M. and Harry B. Helmsley Charitable Trust. The non-dilutive funding will support the advancement of TIX100 into a first-in-human single ascending dose (SAD) study which will commence in January. TIXiMED recently received FDA Investigational New Drug clearance for TIX100, its oral drug candidate that targets thioredoxin-interacting protein (TXNIP), a detrimental protein that is elevated in diabetes and leads to beta cell death and dysfunction. TXNIP inhibition has been demonstrated in mouse models and in humans with type 1 diabetes (T1D) to protect the body’s own insulin producing cells while promoting overall islet cell health. TIX100 is a potent and specific TXNIP inhibitor designed to target this underlying cause of the disease and has been shown in pre-clinical studies to deliver promising effects in diabetes treatment. “ In suppressing TXNIP with TIX100, our aim is to develop a new therapeutic option to promote the patient’s own beta cell survival, insulin production and pancreatic islet health , an approach that is distinct from any currently approved treatments, ” stated Dr. Anath Shalev, TIXiMED founder and Chief Scientific Officer. “ Our SAD study of TIX100 is an exciting step to help bring this new, disease-modifying treatment to market and change the treatment landscape,” Dr. Shalev added. “ TIXiMED is pleased to receive this significant financial support from the Helmsley Charitable Trust. With it, we are poised to rapidly begin our SAD study in human subjects next month ,” said the TIXiMED President, Michael Goodrich. “ Helmsley has a tremendous commitment and a rich history in advancing novel therapies for T1D and we are proud to have them alongside supporting our efforts ,” Mr. Goodrich stated. “ To date, beta-cell targeted therapies that could treat and delay the progression of T1D are an untapped strategy. Therapies such as TIX100 could fulfill an unmet medical need and improve the lives of people living with T1D, ” said Dr. Ben Williams, Program Officer at the Helmsley Charitable Trust. “ This program-related investment will support the efforts of TIXiMED to develop an innovative oral therapeutic for beta cell health and function, bringing T1X100 one step closer to people with T1D, ” Dr. Williams concluded. About TIXiMED Inc. TIXiMED is a clinical stage pharmaceutical company dedicated to developing and commercializing a first-of-its kind oral therapy for type 1 diabetes based on TXNIP inhibition. TIXiMED is the exclusive license holder for the patent surrounding TIX100, a novel, small molecule TXNIP inhibitor, and its derivatives, that has been shown to protect against models of type 1 and type 2 diabetes as well as metabolic dysfunction–associated steatotic liver disease. Visit www.tiximed.com for more information.

引进/卖出

2024-10-21

·生物制药小编

5条肿瘤代谢通路

即使在氧充分的条件下（有氧糖酵解/Warburg效应），癌细胞上调葡萄糖的糖酵解途径形成乳酸，这个过程被认为是恶性肿瘤的标志。代谢活跃的癌细胞导致营养消耗、缺氧、酸性、有毒的代谢物富集的肿瘤微环境，抑制免疫系统。肿瘤细胞代谢与肿瘤微环境（Nat Rev Cancer . 2020 Sep;20(9):516-531）本文简介肿瘤细胞代谢调节的5条信号通路。其他代谢相关文章，请点击下面链接阅读 23种代谢产物与肿瘤免疫 T细胞代谢与功能的关系 1. Hippo Pathway Hippo通路控制细胞增殖、器官大小和组织稳态。它由MAPK家族、MST1/2、LATS1/2以及转录共激活因子YAP和TAZ组成。当该通路被激活时，上游信号磷酸化并激活MST1/2和LATS1/2，从而磷酸化YAP/TAZ。因此，YAP/TAZ通过14-3-3蛋白被隔离在细胞质中，并被E3连接酶β-TRCP降解。 Annu Rev Pathol. 2021 January 24; 16: 299–322 然而，当Hippo信号通路关闭时，YAP/TAZ易位到细胞核，与转录增强相关域(TEAD)转录因子结合，诱导致癌靶基因的表达。 Hippo通路受到广泛的上游调控因子的调控，包括细胞-细胞接触、来自周围环境刺激、Wnt信号传导、GPCR-配体相互作用和各种细胞应激条件。 YAP/TAZ促进糖酵解和谷氨酸代谢 YAP/TAZ活性在许多类型的癌症中都是过度活跃。hHippo通路作为细胞生长的主调节因子，参与了多种代谢过程。YAP/TAZ活性通过直接和间接提高糖酵解酶活性来促进糖酵解。特别是，YAP/TAZ的活性增加了TEAD对GLUT3的表达，并通过FOXC2诱导了HK2的表达。YAP/TAZ还通过Hedgehog信号通路促进LncRNABCAR4的表达，上调HK2和PFKFB3。YAP/TAZ增强谷氨酰胺代谢，增加乳腺癌细胞中谷氨酰胺转运体SLC1A5和SLC7A5的表达。YAP/TAZ和TEAD通过表达氨基酸转运体上调谷氨酰胺和氨基酸代谢。YAP/TAZ诱导谷氨酰胺酶和转氨酶的表达，包括GOT1和PSAT1，它们产生NEAAs和TCA循环中间体。YAP/TAZ积累脂质，直接调节胆汁酸成分，从而增强癌细胞的转移潜能。葡萄糖增强YAP/TAZ的活性细胞周期进程和细胞增殖由营养物质浓度决定。葡萄糖代谢对YAP/TAZ活性有显著影响。高糖水平增加了HSP的葡萄糖通量，产生用于糖基化的UDP-GlcNAc。因此，丰富的葡萄糖诱导YAP O-GlcNAcylation，干扰LATS和βTrCP的相互作用，进而增强YAP/TAZ的活性。在胰腺癌和肝癌中，YAP被O-GlcNAcylation过度激活。 LATS2的糖基化通过干扰乳腺癌中LATS2和MOB1的相互作用来抑制其活性。相反，葡萄糖剥夺诱导的能量应激通过hippo依赖和非依赖的机制抑制YAP/TAZ活性。能量传感器AMPK随着ATP的减少而被激活。AMPK直接磷酸化YAP的丝氨酸61和丝氨酸94，从而阻断YAP-TEAD的相互作用。AMPK通过AMOTL1磷酸化和激活间接抑制YAP。外部激素水平可以调节Hippo通路。脂质激素，如溶血磷脂酸和鞘氨醇-1-磷酸，通过GPCRs抑制该通路，肽激素胰高血糖素增加血糖水平，通过cAMP和PKA激活Hippo通路。脂肪增强YAP/TAZ的活性亚细胞脂质成分也可以调节Hippo通路激酶。SREBP是Hippo通路的上游调控因子。当SREBP被激活时，甲羟戊酸途径增强了RhoAGTPase的香叶酰化。RhoA是一个f-actin的细胞骨架调节因子，而f-actin是一个成熟的LATS激酶的上游因子。因此，癌细胞中脂肪酸代谢的增加会异常激活RhoA，并通过抑制LATS来增强YAP/TAZ的活性。有趣的是，YAP/TAZ在血液系统恶性肿瘤中几乎不表达，而YAP的强制表达已被证明可以介导肿瘤抑制功能。 2. PI3K-AKT/mTOR Pathway 在正常细胞中，细胞的增殖和合成代谢受到外部生长因子（如胰岛素和激素）的微妙调节，PI3K-AKT-mTOR通路是其中一条重要通路。 PI3K/AKT信号通路调节代谢酶。在被胰岛素激活后，AKT通过磷酸化GSK3来抑制糖原合成途径。PI3K/AKT通过代谢酶的翻译后修饰（如磷酸化、糖基化）直接或间接上调糖酵解。例如，AKT磷酸化并激活AS160蛋白，从而增强了GLUT的膜运输。AKT通过抑制磷酸化直接抑制TXNIP，通过抑制内吞作用增加GLUT1/4的膜表达。 AKT还提高了糖酵解酶的效率。AKT通过增加HK2的线粒体整合来磷酸化并激活HK2。AKT使PFKFB磷酸化；这种变化催化果糖-6-磷酸到F-2,6-BP，从而提高糖酵解。AKT信号通路也通过HIF-1α转录因子促进糖酵解。HIF-1激活一些糖酵解组分，包括GLUT。HIF-1诱导LDH促进乳酸分泌和有氧糖酵解。 PI3K/AKT信号通路上调谷氨酰胺和脂肪酸代谢。AKT通过mTORC1增加Myc的翻译，并通过GSK3和FOXO3A抑制Myc的降解。由于MYC调节谷氨酰胺代谢，MYC的激活增加了细胞氮的供应。因此，AKT促进了核苷酸的合成。癌细胞需要从头脂质合成来维持和供应持续的无限细胞分裂所需的膜成分。AKT通过直接磷酸化脂质合成的第一个酶ACLY，影响脂质的新生生物合成过程，从而提高酶的效率。AKT通过ACLY调控增加各种癌症类型中的组蛋白乙酰化 AKT诱导的mTORC1激活增强了SREBP家族的翻译和切割加工。AKT介导的GSK3抑制进一步阻止了SREBP1的降解。因此，了解通过PI3K/AKT信号通路的代谢重编程将阐明PI3K抑制剂对癌症治疗的有效治疗替代方案。 3. Myc Pathway 转录因子c-Myc通过MAX调控基因表达，是癌细胞中最过度活跃的基因之一，位于生长相关信号通路(如EGFR、AKT和GPCRs)的交叉点。 Myc调节与葡萄糖、谷氨酰胺和脂肪酸代谢相关的基因的表达。Myc通过上调糖酵解和谷氨酰胺水解来增强癌细胞的代谢重。Myc诱导许多糖酵解酶(如GLUT、HK2和PFK)，它们催化糖酵解过程相应步骤。 MYC癌基因的激活驱动谷氨酰胺的优先代谢向TCA循环添补反应（Anaplerosis）和随后的氧化磷酸化。MYC癌基因表达的缺失增加了线粒体代谢对葡萄糖的依赖。 4. p53 Pathway P53是最著名的肿瘤抑制基因之一，它影响细胞过程，包括凋亡、细胞周期进程和代谢。p53在细胞应激条件下被激活，如DNA损伤和营养剥夺。根据应激源的类型和强度，它决定了是发生适应还是细胞死亡。p53在转录、翻译和翻译后水平上被调节。p53的稳定性受E3连接酶MDM2的调控。 AMPK磷酸化，乙酰化，从而在能量应激条件下稳定p53。通过上调MDM2来促进p53的降解，p53诱导一个负反馈回路来维持稳态。 p53调节代谢（Cancers 2021, 13, 133） P53减少有氧糖酵解，上调线粒体分解代谢过程，包括脂肪酸氧化(FAO)和OXPHOS；p53转录抑制GLUT1和GLUT4的表达，抑制葡萄糖摄取；抑制TCA循环；增加脂肪酸氧化；增加氧化磷酸化（OXPHOS），积累NADH和FADH2。 5. LKB1/AMPK Pathway AMPK是一种保守性良好的能量传感激酶。AMPK抑制合成代谢途径（脂肪酸合成、mTOR途径），促进分解代谢（糖酵解、Krebs循环、磷酸戊糖途径、脂肪酸氧化和自噬）的细胞过程。因此，AMPK的激活允许细胞承受细胞能量应激条件。与其他代谢蛋白不同，AMPK的调控依赖于AMP和ADP的细胞浓度，但独立于其他代谢中间体。AMP/ATP比值的增加导致AMP相互作用，随后是AMPK的构象变化。在癌症的背景下，应激环境下的AMPK激活，包括缺氧和能量或营养剥夺，赋予了各种癌症的应激抵抗特性。 *红色箭头（激活上调）（Oxid Med Cell Longev . 2019 Oct 31;2019:8730816.） AMPK是一种致癌蛋白还是肿瘤抑制蛋白仍有待确定。在临床环境中，AMPK激活剂，包括2型糖尿病药物二甲双胍和AICAR，被用于抑制癌细胞增殖；然而，AMPK也通过促进原蛋白抗性、迁移和转移作为致癌蛋白。 ACC是AMPK的一个成熟的靶点。ACC在脂肪酸从头合成过程中，ACC介导乙酰辅酶A转化为丙二酰辅酶A。AMPK通过抑制ACC磷酸化来减少ATP的消耗。AMPK降低的脂肪酸合成通量降低了NADPH的消耗。为了满足细胞对脂质代谢物的需求，AMPK通过CD36和其他脂质转运体上调脂肪酸的摄取来维持脂质稳态。蛋白质翻译是高度耗能的，并使用多种合成代谢途径，包括PPP和谷氨酰胺水解。AMPK通过抑制mTORC1和翻译机制，允许癌细胞适应恶劣的营养条件，如葡萄糖剥夺。主要参考文献 Jordan H. Driskill et al，The Hippo Pathway in Liver Homeostasis and Pathophysiology. Annu Rev Pathol. 2021 January 24; 16: 299–322 Robert D. Leone and Jonathan D. Powell, Metabolism of immune cells in cancer, Nat Rev Cancer . 2020 Sep;20(9):516-531 Tambay, V.; Raymond, V.-A.; Bilodeau, M. MYC Rules: Leading Glutamine Metabolism toward a Distinct Cancer Cell Phenotype. Cancers 2021, 13, 4484 : Lahalle, A.; Lacroix, M.; De Blasio, C.; Cissé, M.Y.; Linares, L.K.; Le Cam, L. The p53 Pathway and Metabolism: The Tree That Hides the Forest. Cancers 2021, 13, 133 Francesco Ciccarese et al. LKB1/AMPK Pathway and Drug Response in Cancer: A Therapeutic Perspective,Oxid Med Cell Longev . 2019 Oct 31;2019:8730816.

临床结果

2024-09-19

·贵州医科大学

他们的基础医学创新研究与实验设计荣获全国奖项！

近日，由高等学校国家级实验教学示范中心联席会基础医学组、高等学校基础医学创新创业协同育人工作组主办、中山大学承办的第十届全国大学生基础医学创新研究暨实验设计论坛总决赛暨2024“一带一路”国际大学生医学基础研究创新设计论坛在中山大学举行。共有来自21个国家、204所高校的876支队伍、3216名师生、258位嘉宾与评审专家出席总决赛，办赛规模与参赛人数均创历届之最。经过2天的激烈角逐，总决赛顺利完成各项赛程，圆满落幕。本次总决赛参赛作品涵盖交叉学科等6个学科领域及国际论坛的基础创新研究和实验设计项目。参赛选手们以“汇报+答辩”的方式通过线上和线下形式参加比赛。我校教务处和国家基础医学实验教学中心积极组织，经校赛遴选出15支队伍晋级分区赛。分区赛中我校获二等奖的6支队伍推送参加全国总决赛，分别参加基础临床赛道（3组）、中医药学赛道（2组）以及法医学赛道（1组）。赛场上，选手们精神饱满、思维敏捷、认真严谨，充分展现了我校科教育人在人才培养方面的优秀成果。中医药学赛道李盈锋、刘宇航、李璟琪、饶慧、陈美汐团队的《绞股蓝总皂苷通过SIRT1减轻CUMS诱导大鼠的海马氧化应激并促进线粒体自噬以改善抑郁样行为》（指导老师：吴宁、修江帆）、中医药学赛道左键操、蒋卓君、罗海兰、唐艳、冯煜璇团队的《丹参酮IIA调控IRE1α/TXNIP/NLRP3改善2型糖尿病骨质疏松症的分子机制研究》（指导老师：禹文峰、袁桃花）获得银奖及“最佳团队合作奖”；基础临床赛道李涛、崔家田、赵思润、汤薪照、邹东岑团队的《慢性糖尿病抑制Syntaxin 17表达导致自噬体与溶酶体融合障碍加重心肌缺血再灌注损伤》（指导老师：陈超、胡廷菊）、基础临床赛道罗炜思、王顺雯、吴国静、李志宏、杨燕花团队的《黑磷纳米片通过促进自噬和清除ROS改善卵巢衰老的作用及机制研究》（指导老师：何美娜、张拓）、法医学赛道张慧、赵骏诚、安南、刘源卿团队的《美托咪酯在大鼠体内的毒代动力学及法医学应用研究》（指导老师：陈顺琴、刘玉波）获得铜奖。全国大学生基础医学创新研究暨实验设计论坛暨2024“一带一路”国际大学生医学基础研究创新设计论坛是全国基础医学教育领域影响力最大的大学生创新大赛之一。通过本次比赛我校学生展现出了较扎实的理论功底、优秀的创新精神和实践能力，促进了高校间的交流与合作。来源：基础医学院教务处作者：肖鑫排版：张达安编辑：李菡逸一审：李牧二审：钱禾三审：陈颖往期回顾 RECENTLY RELEASED 看看你的MBTI是哪座校园建筑？如果你有社恐、拖延症…？这样做，让它通通out！ GMUer一起来游玩！贵州医科大学版权所有期待投稿合作邮箱：gmctougao@163.com