检索结果-内蒙古大学图书馆

txnip knockdown ameliorates hepatic ischemia/reperfusion injury by inhibiting apoptosis and improving mitochondrial dysfunction via HIF-1α

引用

MOLECULAR AND CELLULAR BIOCHEMISTRY 2025年第4期480卷 2291-2300页

作者： Zhang, Yong Lv, Jianrui Bai, Jian Zhang, Xue Wu, Gang Lei, Xiaoming Li, Wei Zhang, Zhenni Xi An Jiao Tong Univ Dept Anesthesia Affiliated Hosp 2 157 West 5th Rd Xian 710004 Shaanxi Peoples R China Capital Med Univ Dept Gen Surg Xuanwu Hosp Beijing 100032 Peoples R China Capital Med Univ Beijing Friendship Hosp Dept Gen Practice Beijing 100050 Peoples R China

This study aims to investigate whether thioredoxin-interacting protein (txnip) regulates cell viability, cell apoptosis and mitochondrial damage in OGD/R-induced hepatocytes and to explore its underlying mechanism. AML12 cells were cultured under oxygen-glucose deprivation/reperfusion (OGD/R) conditions. txnip mRNA was detected using qRT-PCR, and the txnip protein was analyzed using western blotting. txnip-targeted short hairpin RNA (sh-txnip) lentivirus was used to infect the AML12 cells. CCK8 and TUNEL assays were applied to detect cell viability and apoptosis, respectively. DCFH-DA probe was used to determine reactive oxygen species (ROS) release level, and JC-1 probe was used to evaluate mitochondrial membrane potential (MMP). The localization of txnip and HIF-1 alpha was observed using immunofluorescence. Our results showed that txnip markedly increased in AML12 cells treated with OGD/R. txnip knockdown increased cell viability and reduced cell apoptosis under OGD/R treatment. Moreover, MMP significantly increased and ROS release decreased in cells after txnip knockdown under OGD/R treatment. Additionally, txnip knockdown markedly increased the expression of HIF-1 alpha. HIF-1 alpha exhibited nuclear translocation following OGD/R induction, and txnip knockdown further promoted it. Compared with the OGD/R + sh-txnip group, HIF-1 alpha agonist ML228 inhibited cell apoptosis and ROS release, and increased MMP. However, HIF-1 alpha inhibitor PX478 had the opposite effect. In summary, txnip deletion ameliorated AML12 cell injury caused by OGD/R via promoting HIF-1 alpha expression and nuclear translocation, manifested by inhibiting cell apoptosis and alleviating mitochondrial dysfunction.

关键词： Hepatic Ischemia/reperfusion injury txnip HIF-1 alpha Mitochondria Apoptosis

来源：评论

学校读者我要写书评

暂无评论

TXM-CB13 Improves the Intestinal Mucosal Barrier and Alleviates Colitis by Inhibiting the ROS/txnip/TRX/NLRP3 and TLR4/MyD88/NF-κB/NLRP3 Pathways

引用

INFLAMMATION 2025年 1-13页

作者： Cao, Ruijie Zhou, Jinhui Liu, Jiale Wang, Yaxuan Dai, Yandong Jiang, Yun Yamauchi, Akira Atlas, Daphne Jin, Tiancheng Zhou, Jiedong Wang, Cuixue Tan, Qihuan Chen, Yifei Yodoi, Junji Tian, Hai Shaoxing Univ Med Coll Dept Basic Med Shaoxing Peoples R China Misugi Kai Sato Hosp Breast Ctr Dept Breast Surg Hirakata Osaka Japan Hebrew Univ Jerusalem Inst Life Sci Dept Biol Chem IL-91904 Jerusalem Israel Kyoto Univ Inst Virus Res Dept Biol Response Lab Infect & Prevent Kyoto Japan Jiaozhimei Biotechnol Shaoxing Co Ltd Shaoxing Peoples R China

The activation of inflammasomes (NLRP3 and NLRP1) is central to the pathogenesis of inflammatory bowel disease (IBD). Here we examined the protective effects of a thioredoxin-mimetic peptide CB13 (TXM-CB13), known for its antioxidative stress and anti-inflammatory properties. We examined the effects of TXM-CB13 on dextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-induced NLRP3 inflammasome activation in RAW264.7 macrophages. TXM-CB13 appeared to alleviate symptoms of DSS-induced colitis and to significantly suppress the protein and mRNA levels of NLRP3, Mlck, and IL-1 beta in colonic tissues. Additionally, TXM-CB13 treatment increased the levels of the intestinal barrier proteins Occludin, ZO-1, and NLRP1, as shown through immunohistochemistry and Western blot analysis. In vitro, TXM-CB13 inhibited LPS-induced TLR4 signaling, reducing MyD88 levels and consequently attenuating the activation of the NF-kappa B pathways, including p-I kappa B-alpha/I kappa B-alpha and p-NF-kappa B-p65/NF-kappa B-p65. This inhibition further reduced the activation of the NLRP3 inflammasome components, NLRP3, ASC, Caspase-1, GSDMD, and IL-1 beta. In addition, TXM-CB13 prevented the ROS-mediated dissociation of txnip from TRX, inhibiting NLRP3 activation. These findings suggest that TXM-CB13 is a potential therapeutic candidate for IBD through its modulation of the TLR4/MyD88/NF-kappa B/NLRP3 and ROS/txnip/TRX/NLRP3 pathways.

关键词： TXM-CB13 Inflammatory bowel disease NLRP3 txnip NF-kappa B

来源：评论

学校读者我要写书评

暂无评论

Gynostemma pentaphyllum (Thunb.) Makino Affects Autophagy and Improves Diabetic Peripheral Neuropathy Through txnip-Mediated PI3K/AKT/mTOR Signaling Pathway

引用

APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY 2025年第2期197卷 1209-1224页

作者： Jia, Chao Zhao, XueMin Song, MeiJia Sun, XinYue Zibo Hosp Tradit Chinese Med Dept Endocrinol Zibo 255300 Shandong Peoples R China Zibo Hosp Tradit Chinese Med Dept Pharmaceut Zibo 255300 Shandong Peoples R China Zibo Hosp Tradit Chinese Med Dept Encephalopathy Zibo 255300 Shandong Peoples R China

txnip is closely associated with diabetic peripheral neuropathy (DPN). Gynostemma pentaphyllum (Thunb.) Makino (GP), a perennial herb with five leaves, is considered to have medicinal values. However, it is unknown whether GP alleviates DPN by modulating txnip-mediated autophagy. The aim of this study was to evaluate the effect of GP on Schwann cell injury during DPN and to investigate the mechanism of GP in DPN for the first time. High-fat diet-fed GK rats and high-glucose-cultured RSC96 cells were used to establish DPN models. The effects of GP on DPN were investigated by blood glucose assay, neurological function assay, pathology assay, and immunohistochemistry. To investigate the effect of GP on autophagy and upstream PI3K/AKT/mTOR signaling pathway in Schwann cells, Western blot and immunofluorescence assay were performed on RSC96 cells to detect the expression of beclin-1 and LC3. Western blot method was used to detect the expression of PI3K, p-Akt/Akt, p-mTOR/mTOR, and RT-qPCR method and was used to detect the expression of PI3K. Apoptosis was detected by flow cytometry. The effects of txnip on the above indicators were also detected in RSC96 cells. Finally, the mechanism of GP regulation of autophagy and apoptosis in RSC96 cells was verified. GP reduced blood glucose level, attenuated peripheral nerve myelin damage, and improved nerve function in DPN rats. In addition, GP enhanced autophagy activity and reduced apoptosis in RSC96 cells. GP promoted autophagy by regulating txnip-mediated PI3K/AKT/mTOR signaling pathway, and GP reduced apoptosis in RSC96 cells by promoting cellular autophagy. GP attenuates DPN myelin damage in RSC96 cells by enhancing autophagy, and its mechanism may be related to the inhibition of PI3K/AKT/mTOR signaling pathway by up-regulating the expression of txnip.

关键词： Apoptosis Autophagy Diabetic peripheral neuropathy txnip Schwann cells

来源：评论

学校读者我要写书评

暂无评论

Bone Marrow Mesenchymal Stem Cell-Originated Exosomes Curb Oxidative Stress and Pyroptosis Triggered by Ovarian Ischemia/Reperfusion via the txnip/NLRP3 Inflammasome Pathway

引用

APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY 2025年 1-22页

作者： Xu, Min Don, Min Chen, Yiyuan Zhang, Mingzhe Zunyi Med Univ Affiliated Hosp Dept Reprod Med 149 Dalian Rd Zunyi 563000 Guizhou Peoples R China

Mesenchymal stem cells (MSCs) and their secreted exosomes (Exos) have attracted much interest for their potential against ischemia/reperfusion injury (IRI). In the present research, we employed rat ovarian ischemia/reperfusion injury (OIRI) model and hypoxia/reoxygenation (H/R) model of primary rat ovarian granulosa cells (RGCs) to investigate whether BMSC-Exos could alleviate OIRI. Our data suggested that administration of BMSCs in rats significantly reduced OIRI-resultant histopathological changes, oxidative stress, inflammation, and pyroptosis. In addition, BMSCs downregulated the expression of proteins related to the txnip/NLRP3 inflammasome pathway. Based on in vitro experiments, BMSC-Exos could be internalized by RGCs and curbed oxidative stress and pyroptosis in H/R-injured RGCs. This effect may be due to the regulation of txnip/NLRP3 inflammasome pathway. Remarkably, our in vivo data were in concordance with our in vitro results, suggesting that BMSC-Exos suppressed OIRI-induced oxidative stress and pyroptosis via the txnip/NLRP3 inflammasome pathway. Overall, these results demonstrate good therapeutic efficacy of BMSC-Exos for treating OIRI, which may provide experimental evidence for the potential clinical benefits of BMSC-Exos for ovarian protection.

关键词： Exosomes Mesenchymal stem cells Ovarian ischemia-reperfusion Ovarian granulosa cells txnip NLRP3 inflammasome Oxidative stress Pyroptosis

来源：评论

学校读者我要写书评

暂无评论

Nobiletin regulates the proliferation and migration of ovarian cancer A2780 cells via DPP4 and txnip

引用

NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY 2025年第2期398卷 1483-1495页

作者： He, Xiuzhen Dou, Lu Wang, Jie Xia, Lili Miao, Jiawei Yan, Yongbo Chongqing Three Gorges Med Coll Dept Basic Med Chongqing 404120 Peoples R China Chongqing Three Gorges Med Coll Key Lab Chongqing 404120 Peoples R China Chongqing City Wanzhou Dist Shanghai Hosp Surg 3 Chongqing 404120 Peoples R China Chongqing Three Gorges Med Coll Peoples Hosp Pharm Dept 27Guoben Rd Chongqing 404197 Peoples R China

Nobiletin is an active compound extracted from citrus fruits. Research has indicated that nobiletin has a potential inhibitory effect on ovarian cancer (OV). However, the mechanism of action remains unclear. The OV A2780 cells were treated using nobiletin, cell viability was examined using a cell counting kit-8 experiment, and cell migration was examined with a wound healing experiment. Nobiletin targets were retrieved from target databases. Differentially expressed genes (DEG) and weighted gene co-expression network analysis (WGCNA) were conducted on GSE26712 (OV). The intersection of the critical genes for nobiletin's action on OV and gene enrichment and immune infiltration analyses were performed. The Cancer Genome Atlas-OV data and molecular docking helped validate the findings. After adding nobiletin, cell viability and migration significantly decreased (P < 0.01). A total of 88 nobiletin targets and 1288 DEG were identified. The intersection genes were enriched inflammatory response and response to hypoxia. The most related module obtained from WGCNA contained 414 genes (correlation coefficient = 0.77, P < 0.01). DPP4 and txnip were recognized as the hub genes. The abundance of macrophages M2 and mast cells activated significantly enhanced with increased DPP4 expression (P < 0.05). The binding energy between DPP4/txnip and nobiletin was - 7.012/ - 7.184 kcal/mol, forming 5/2 hydrogen bonds. Nobiletin effectively suppresses the viability and migration of OV A2780 cells. In this process, DPP4 and txnip are the key target, immune regulation, and oxidative stress playing significant roles.

关键词： Nobiletin Ovarian cancer DPP4 txnip Molecular docking

来源：评论

学校读者我要写书评

暂无评论

Rocaglamide reprograms glucose metabolism in erythroleukemic cells via c-MYC transcriptional regulation of txnip and HK2

引用

JOURNAL OF ETHNOPHARMACOLOGY 2025年 339卷 119145页

作者： Song, Jialei Liu, Wuling Xiao, Xiao Song, Jingrui Wang, Chunlin Gajendran, Babu Wei, Xuenai Yang, Changfu Chen, Yunzhi Yang, Yiying Huang, Lei Song, Junrong Ben-David, Yaacov Li, Yanmei Guizhou Univ Tradit Chinese Med Sch Basic Med Guiyang 550025 Peoples R China Guizhou Univ Tradit Chinese Med Key Lab Mol Biol Guiyang 550025 Peoples R China Guizhou Univ Tradit Chinese Med Sch Pharm Guiyang 550025 Peoples R China Nat Prod Res Ctr Guizhou Prov Guiyang 550014 Peoples R China Guizhou Med Univ State Key Lab Funct & Applicat Med Plants Guiyang 550014 Peoples R China Guizhou Med Univ Sch Pharmaceut Sci Guiyang 550025 Peoples R China

Ethnopharmacological relevance: The theory of traditional Chinese medicine (TCM) views leukemia as an imbalance between cell growth and death mainly caused by blood stasis. Medicinal plants Aglaia Lour. (family Meliaceae) are traditionally used as folk medicine in China. It possesses the effects of removing blood stasis and swelling for treatment of cancer. Rocaglamide (RocA) is the main active phytochemical component of the genus Aglaia Lour. Possessing highly anti-leukemia properties. However, the molecular mechanisms by which RocA exerts its anti-growth effect on erythroleukemia cells are largely unknown. Aim of the study: This study aimed to explore the underlying mechanism and glucose metabolism regulation effects of RocA responsible for its anti-erythroleukemia activity. Materials and methods: Human erythroleukemic cells were tested for glucose metabolism and treated with glucose deprivation and RocA. MTT assay, cell cycle and apoptosis were used to elucidate growth inhibition. Glucose uptake, glucose consumption and lactate production were evaluated for identification of glucose metabolism. Luciferase assay and ChIP were used to examine the transcriptional activity of c-MYC on the conserved E-boxes binding of the txnip ( thioredoxin-interacting protein) and HK2 ( hexokinase 2) genes. siRNA, shRNA and exogenous transfection were employed to elucidate the effects of txnip and HK2 on glucose metabolism. Results: We find that glucose deprivation results in growth inhibition, cell cycle arrest and extensive apoptosis in erythroleukemic cells accompanied by downregulation of c-MYC and HK2, responsible for glucose metabolism. The similar results emerged in RocA treated erythroleukemic cells in presence of glucose. RocA is shown to decrease glucose uptake, glucose consumption and lactate production. Mechanistically, RocA dramatically increases txnip expression through interference with c-MYC binding to the promoter of the txnip gene. RocA also represses c-MYC transcr

关键词： Rocaglamide c-MYC txnip HK2 Glucose metabolism Erythroleukemic cell proliferation

来源：评论

学校读者我要写书评

暂无评论

Bone marrow mesenchymal stem cell transplantation protects rats from myocardial infarction by regulating txnip/NLRP3 pathway-mediated inflammation and fibrosis

引用

MOLECULAR & CELLULAR TOXICOLOGY 2025年第1期21卷 129-138页

作者： Bai, JianNan Wang, Cong Yu, HongQiang Wang, QingChao Zhang, JinFeng Shao, DanDan Yu, ZhiQiang Meng, Bo Li, You Daqing Peoples Hosp Dept Cardiol 213 Jianshe Rd Daqing 163711 Heilongjiang Peoples R China

BackgroundBone marrow mesenchymal stem cells (BMSCs) may be a promising target in the treatment of myocardial infarction (MI). However, the underlying molecular mechanisms of BMSC therapy remain *** study sought to evaluate the efficacy of direct intramyocardial transplantation of BMSCs in a mouse model of *** BMSCs were transfected with small interfering RNA or overexpression plasmid targeting txnip. The viability, proliferation, and apoptosis of BMSCs after hypoxia treatment were detected by MTT method, EdU analysis, and flow cytometry, respectively. A mouse model of MI was constructed, after which BSMCs were injected intramyocardially immediately. Cardiac ultrasound, HE staining, TUNEL staining and ELISA, IHC analysis, and Western blot were adopted to evaluate the effects of BSMC therapy on cardiac function, myocardial inflammation, and fibrosis in *** vitro experiments reported that ablating txnip increased viability and inhibited apoptosis of hypoxia-treated BMSCs while overexpressing txnip did the opposite. In vivo results stated that BSMCs improved cardiac function, myocardial inflammation, and fibrosis after MI, which was further improved by silencing txnip but reversed by overexpressing txnip. Meanwhile, in vivo cell tracking experiments showed that the retained BMSCs in the myocardium decreased after transplantation, and txnip depletion promoted the survival of BMSCs in MI mice, whereas txnip overexpression did the *** conclusion, BMSC transplantation improves cardiac function, myocardial inflammation, and fibrosis after MI by regulating the txnip/NLRP3 pathway.

关键词： Bone marrow mesenchymal stem cells txnip NLRP3 Myocardial infarction Heart failure

来源：评论

学校读者我要写书评

暂无评论

A novel application perspective of the clinical-used drug verapamil on osteoporosis via targeting txnip

引用

JOURNAL OF ORTHOPAEDIC TRANSLATION 2025年 50卷 158-173页

作者： Cao, Xiankun Rong, Kewei Li, Yinghua Zhang, Pu Liu, Kexin Cui, Lei Fu, Shaotian Hua, Qi Yang, Xiao Zhang, Hang Cheng, Xiaofei Ma, Peixiang Zhao, Jie Qin, An Shanghai Jiao Tong Univ Shanghai Peoples Hosp 9 Dept Orthoped Surg Shanghai Key Lab Orthoped ImplantsSch Med Shanghai 200011 Peoples R China Shanghai Fudan Univ Shanghai Peoples Hosp 5 Sch Med Shanghai Med SchCent Lab Shanghai 200011 Peoples R China Guangxi Med Univ Guangxi Collaborat Innovat Ctr Biomed Guangxi ASEAN Collaborat Innovat Ctr Major Dis Pre Guangxi Key Lab Regenerat Med Nanning 530021 Guangxi Peoples R China

Background: RANKL and SCLEROSTIN antibodies have provided a strong effective choice for treating osteoporosis in the past years, which suggested novel molecular target identification and therapeutic strategies development are important for the treatment of osteoporosis. The therapeutic effect of verapamil, a drug previously used for cardiovascular diseases, on diabetes was due to the inhibition of txnip expression, which has also been reported as a target in mice osteoporosis. Whether verapamil-inhibited txnip expression is related to osteoporosis and how it works on the molecular level is worthy to be explored. Methods: The polymorphism genotyping analysis was performed on patients with different degrees of osteoporosis. The responsiveness of bone marrow-derived macrophage cells (bone marrow-derived mesenchymal stem cells) to verapamil was evaluated by CCK-8, TRAP staining assay (ALP and AR staining assay), Bone Resorption Assay, and RNA-Sequencing. The expression and cytoplasmic efflux of ChREBP were determined by western blotting and immunofluorescence. Bilateral ovariectomy models were created, rescued by verapamil injection and the effectiveness was evaluated by Micro-CT and Histological analysis. Results: Here we discovered that rs7211 single nucleotide polymorphism (SNP) of txnip is closely associated with increased femur neck bone mineral density (BMD) and decreased osteoporosis rate, suggesting the importance of txnip in the development of osteoporosis. Verapamil suppresses txnip expression, reduces bone turnover rate and thus rescues ovariectomy-induced mice bone loss. Mechanistically, verapamil promoted ChREBP cytoplasmic efflux, regulated Ppar gamma expression both mediating txnip-MAPK, NF-kappa B axis in osteoclasts, and suppressed the ChREBP-txnip-Bmp2 axis in osteoblasts. Conclusions: The results of our study show the correlation of rs7211 txnip-T allele with Chinese increased femur neck BMD and decreased osteoporosis rate. In addition, verapamil can

关键词： Bone turnover ChREBP Osteoporosis txnip Verapamil

来源：评论

学校读者我要写书评

暂无评论

Nicotinamide mononucleotide ameliorates hypertriglyceridemia pancreatitis via NAD+/SIRT1-mediated txnip suppression and NOTCH pathway for accelerated repair-associated processes

引用

INTERNATIONAL IMMUNOPHARMACOLOGY 2025年 155卷 114620页

作者： Duan, Hongtao Zhang, Rui Asikaer, Aiminuer Pan, Liang Wang, Shui Huang, Kuilong Lou, Deshuai Wang, Yuanqiang Lin, Zhihua Shen, Yan Chongqing Univ Technol Sch Pharm & Bioengn Chongqing 405400 Peoples R China Chongqing Coll Tradit Chinese Med Chongqing 402760 Peoples R China Guizhou Prov Peoples Hosp Dept Pharm Guiyang 550002 Peoples R China Chongqing Univ Educ Sch Biol & Chem Engn Chongqing Key Lab Med Resources Three Gorges Reser Chongqing 400067 Peoples R China

Background & Aims: Acute pancreatitis (AP) is a life-threatening condition, and hypertriglyceridemia (HTG) is recognized as a factor exacerbating AP and impeding pancreatic regeneration. Nicotinamide mononucleotide (NMN), a precursor in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), is extensively utilized to restore NAD+ levels. However, the impact of NMN on HTG-AP has not been previously addressed, which prompted our investigation into its effects and underlying mechanisms in this study. Methods & Results: Here, through bioinformatics analysis and in vivo experiments, we identified abnormalities in the thioredoxin system. In vitro studies revealed that NMN rescued oleic acid (OA)- and palmitic acid (PA)-induced mitochondrial dysfunction and cellular injury in pancreatic acinar cells by suppressing thioredoxininteracting protein (txnip) through NAD+/sirtuin 1 (SIRT1) signaling. Repeated administration of NMN significantly ameliorated P407 and caerulein (CER)-induced pancreatic injury and dysfunction in mice. Consistently, NMN exhibited the potential to reduce inflammatory responses, lower serum lipid levels, and mitigate the accumulation of reactive oxygen species (ROS). More importantly, sustained NMN treatment inhibited the NOTCH pathway and promoted M2-type macrophage dominance during the pancreatic repair phase, influencing early or late macrophage polarization, which significantly enhanced inflammation resolution. As expected, in vitro models using mouse bone marrow-derived macrophage (BMDM), RAW 264.7, and THP-1 cells confirmed that NMN influences macrophage phenotype through the NOTCH pathway. Conclusions: Therefore, NMN ameliorates pancreatic acinar cell injury via NAD+/SIRT1-mediated txnip suppression and may influence macrophage polarization by inhibiting NOTCH activation, offering a novel therapeutic strategy for the treatment and repair of HTG-AP.

关键词： Hypertriglyceridemia pancreatitis Nicotinamide mononucleotides SIRT1 txnip NOTCH

来源：评论

学校读者我要写书评

暂无评论

CircHIPK2 recruits SRSF1 to increase txnip mRNA stability and promotes autophagy-dependent ferroptosis and apoptosis in myocardial ischemia-reperfusion injury

引用

JOURNAL OF CARDIOTHORACIC SURGERY 2025年第1期20卷 1-13页

作者： Zhang, Zhu Hao, Jinqi Qiao, Qinghong Song, Junting Yu, Yanqin Baotou Med Coll Affiliated Hosp 1 Dept Cardiol 1 41 Linyin Rd Baotou 014010 Inner Mongolia Peoples R China Baotou Med Coll Sch Publ Hlth Baotou Peoples R China

BackgroundMyocardial ischemia/reperfusion injury (MIRI) secondary to acute myocardial infarction (AMI) can lead to cardiomyocyte death and impaired cardiac function. Studies have confirmed that circular RNAs (circRNAs) play an important role in MIRI. In this study, the role and mechanism of circHIPK2 in MIRI were *** cardiac myocytes (HCM) were cultured under Hypoxia/Reoxygenation (H/R) condition to establish a MIRI model in vitro. Expression of circHIPK2, SRSF1 and txnip was assessed using RT-qPCR. Protein levels of autophagy markers (LC3II/LC3I, Beclin1, p62) and ferroptosis markers (GPX4, FTH1, ACSL4) were detected by Western blot. Cell viability and apoptosis were assessed by CCK-8 and flow cytometry. Levels of oxidative stress markers (MDA, SOD) and inflammatory factors (IL-6, IL-1 beta, TNF-alpha) were tested by ELISA assay. Iron concentration was measured with an iron detection kit. Location of circHIPK2 in cells was detected by RNA-nucleosome separation assay. RIP and ChIP assays verified the relationship between circHIPK2, SRSF1 and txnip. txnip mRNA stability was dertermined by actinomycin D. Infarct area was examined by TTC staining in myocardial ischemia/reperfusion (I/R) mouse model. HE staining evaluated myocardial ***2 was increased in H/R-induced HCM cells. CircHIPK2 downregulation suppressed oxidative stress, inflammatory factors and autophagy-dependent ferroptosis in HCM cells induced by H/R. Additionally circHIPK2 recruited SRSF1 to target txnip and stabilized txnip mRNA expression. We further demonstrated that txnip upregulation overturned the therapeutic effects of circHIPK2 silencing on H/R model cells. In vivo, downregulation of circHIPK2 improved myocardial dysfunction caused by I/*** results demonstrate that circHIPK2 contributes to MIRI through inducing oxidative stress and autophagy-dependent ferroptosis via SRSF1/txnip axis, offering new insights into MIRI treatment.

关键词： CircHIPK2 SRSF1 txnip Ferroptosis Myocardial ischemia-reperfusion injury

来源：评论

学校读者我要写书评

暂无评论

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案：

请选择收藏分类：

通借通还

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：