Redox Report最新文献_第9页

CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway. CEACAM5通过JAK/ stat6依赖通路诱导气道上皮细胞铁凋亡和自噬，从而加重哮喘。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-23 DOI: 10.1080/13510002.2024.2444755

Si Liu, Li Chen, Yunxiao Shang

{"title":"CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway.","authors":"Si Liu, Li Chen, Yunxiao Shang","doi":"10.1080/13510002.2024.2444755","DOIUrl":"10.1080/13510002.2024.2444755","url":null,"abstract":"Objectives: Asthma, a prevalent chronic disease, poses significant health threats and burdens healthcare systems. This study focused on the role of bronchial epithelial cells in asthma pathophysiology.Methods: Bioinformatics was used to identify key asthmarelated genes. An ovalbumin-sensitized mouse model and an IL-13-stimulated Beas-2B cell model were established for further investigation.Results: Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) was identified as a crucial gene in asthma. CEACAM5 expression was elevated in asthmatic mouse lung tissues and IL-13-stimulated Beas-2B cells, primarily in bronchial epithelial cells. CEACAM5 induced reactive oxygen species (ROS), lipid peroxidation, and ferroptosis. Interfering with CEACAM5 reduced ROS, malondialdehyde levels, and enhanced antioxidant capacity, while inhibiting iron accumulation and autophagy. Overexpression of CEACAM5 in IL-13-stimulated cells activated the JAK/STAT6 pathway, which was necessary for CEACAM5-induced autophagy, ROS accumulation, lipid peroxidation, and ferroptosis.Conclusion: CEACAM5 promotes ferroptosis and autophagy in airway epithelial cells via the JAK/STAT6 pathway, exacerbating asthma symptoms. It represents a potential target for clinical treatment.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2444755"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-invasive electron paramagnetic resonance imaging detects tumor redox imbalance induced by ferroptosis. 无创电子顺磁共振成像检测由铁下垂引起的肿瘤氧化还原失衡。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-21 DOI: 10.1080/13510002.2025.2454887

Kazuhiro Kato, Hironobu Yasui, Hideo Sato-Akaba, Miho C Emoto, Hirotada G Fujii, Maciej M Kmiec, Periannan Kuppusamy, Masaki Nagane, Tadashi Yamashita, Osamu Inanami

{"title":"Non-invasive electron paramagnetic resonance imaging detects tumor redox imbalance induced by ferroptosis.","authors":"Kazuhiro Kato, Hironobu Yasui, Hideo Sato-Akaba, Miho C Emoto, Hirotada G Fujii, Maciej M Kmiec, Periannan Kuppusamy, Masaki Nagane, Tadashi Yamashita, Osamu Inanami","doi":"10.1080/13510002.2025.2454887","DOIUrl":"10.1080/13510002.2025.2454887","url":null,"abstract":"Targeting ferroptosis, cell death caused by the iron-dependent accumulation of lipid peroxides, and disruption of the redox balance are promising strategies in cancer therapy owing to the physiological characteristics of cancer cells. However, the detection of ferroptosis using in vivo imaging remains challenging. We previously reported that redox maps showing the reduction power per unit time of implanted tumor tissues via non-invasive redox imaging using a novel, compact, and portable electron paramagnetic resonance imaging (EPRI) device could be compared with tumor tissue sections. This study aimed to apply the EPRI technique to the in vivo detection of ferroptosis. Notably, redox maps reflecting changes in the redox status of tumors induced by the ferroptosis-inducing agent imidazole ketone erastin (IKE) were compared with the immunohistochemical images of 4-hydroxynonenal (4-HNE) in tumor tissue sections. Our comparison revealed a negative correlation between the reducing power of tumor tissue and the number of 4-HNE-positive cells. Furthermore, the control and IKE-treated groups exhibited significantly different distributions on the correlation map. Therefore, redox imaging using EPRI may contribute to the non-invasive detection of ferroptosis in vivo.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2454887"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143010806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sodium-glucose cotransporter 2 inhibitors ameliorate glutathione cysteine ligase modifier-mediated oxidative stress and subsequent ferroptosis in proximal tubules of diabetic kidney disease. 钠-葡萄糖共转运蛋白2抑制剂改善糖尿病肾病近端小管中谷胱甘肽半胱氨酸连接酶修饰物介导的氧化应激和随后的铁下垂。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-28 DOI: 10.1080/13510002.2025.2528334

Yi-Chun Tsai, Jiun-Chi Huang, Ping-Shaou Yu, Mei-Chuan Kuo, Ling-Yu Wu, Wei-An Chang, Shang-Jyh Hwang, Ya-Ling Hsu

{"title":"Sodium-glucose cotransporter 2 inhibitors ameliorate glutathione cysteine ligase modifier-mediated oxidative stress and subsequent ferroptosis in proximal tubules of diabetic kidney disease.","authors":"Yi-Chun Tsai, Jiun-Chi Huang, Ping-Shaou Yu, Mei-Chuan Kuo, Ling-Yu Wu, Wei-An Chang, Shang-Jyh Hwang, Ya-Ling Hsu","doi":"10.1080/13510002.2025.2528334","DOIUrl":"10.1080/13510002.2025.2528334","url":null,"abstract":"Objectives: Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease. The precise molecular mechanism of ferroptosis, an iron-dependent and non-apoptotic form of regulated cell death, remains poorly understood in DKD, as does the impact of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on ferroptosis-mediated DKD.Methods: This study used bulk RNA sequencing, in vitro and in vivo models, and human kidney samples to explore the molecular mechanisms involved in oxidative stress and ferroptosis in the proximal tubule (PT) of DKD.Results: High glucose (HG) induced features of ferroptosis in HK-2 cells. Transcriptome analysis of primary PT cells from diabetic patients indicated that glutathione cysteine ligase modifier (GCLM) subunit is involved in ferroptosis. Immunohistochemical staining revealed that db/db mice and diabetic patients had lower glutathione peroxidase 4 and GCLM expression in the PT. Suppression of GCLM enhanced ferroptosis, whereas GCLM overexpression mitigated HG-induced ferroptosis in HK-2 cells. Antioxidants reduced oxidative stress and ferroptosis in both in vitro and in vivo models of DKD. Furthermore, SGLT2i attenuated PT ferroptosis in these models and improved DKD by increasing GCLM expression.Conclusion: SGLT2i reduced ferroptosis in PT by boosting GCLM expression, thereby slowing DKD progression, revealing that GCLM has the potential against DKD.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2528334"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Melatonin inhibits ferroptosis in myocardial ischemia/reperfusion injury by inhibiting the ATM/p53 signaling pathway. 褪黑素通过抑制ATM/p53信号通路抑制心肌缺血再灌注损伤中的铁下垂。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-11-03 DOI: 10.1080/13510002.2025.2583802

Peng Wang, Di Wang, Zhen Lv, Peng Zhang, Xiangting Su, Ting Zhao, Yan Dong, Shengqiang Li

{"title":"Melatonin inhibits ferroptosis in myocardial ischemia/reperfusion injury by inhibiting the ATM/p53 signaling pathway.","authors":"Peng Wang, Di Wang, Zhen Lv, Peng Zhang, Xiangting Su, Ting Zhao, Yan Dong, Shengqiang Li","doi":"10.1080/13510002.2025.2583802","DOIUrl":"10.1080/13510002.2025.2583802","url":null,"abstract":"Background: Melatonin is a powerful free radical scavenger, with cardioprotective effects; however, the mechanism of this cardioprotective activity remains unclear. We hypothesized that melatonin inhibits ferroptosis and protects cardiomyocytes through suppression of the ataxia telangiectasia mutated (ATM)/p53 signaling pathway and reduction of lipid peroxidation.Methods: Forty-two rat hearts were randomly assigned to a control group or one of six experimental groups (I/R, I/R + melatonin, I/R + melatonin + chloroquine diphosphate5, I/R + chloroquine diphosphate1, I/R + chloroquine diphosphate5, I/R + chloroquine diphosphate25). Thirty C57/BL6 male mice were assigned to 5 groups, with the same grouping as rats. The hearts were reperfused, after which the levels of creatine kinase MB, malondialdehyde, superoxide dismutase, iron, and glutathione/ glutathione oxidized were measured. Triphenyl tetrazolium chloride (TTC) staining, Hematoxylin and eosin staining, X-ray electron microscopy, western blotting, and immunofluorescence were performed to evaluate the effects of melatonin treatment on the pathology, microstructure, and antioxidant enzymes of the myocardium (ferritin heavy chain 1 (FTH1), SLC7A11 (XCT), superoxide dismutase-2 (SOD-2), and glutathione peroxidase 4 (GPX4), p53, and p-p53).Results: Ischemia/reperfusion increased myocardial lipid peroxidation, iron and p53 contents, as well as damage to the myocardial pathology and mitochondrial structure, and decreased the expression levels of antioxidant enzymes. Melatonin treatment alleviated these effects, which were reversed by chloroquine diphosphate.Conclusions: These findings suggest that melatonin pretreatment protects cardiomyocytes from I/R injury by inhibiting cell ferroptosis via suppression of the ATM/p53 signaling pathway.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2583802"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12584827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145438841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sesamin alleviates drug-induced hepatotoxicity via autophagy enhancement and ferroptosis inhibition. 芝麻素通过增强自噬和抑制铁下垂来减轻药物引起的肝毒性。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-11-18 DOI: 10.1080/13510002.2025.2588863

Jingyi Ren, Ziyi Wang, Yadong Zhang, Huanting Pei, Rui Wen, Zhenao Zhang, Siqi Zhu, Xiaoya Sun, Bowen Yin, Shenghe Li, Yuxia Ma

{"title":"Sesamin alleviates drug-induced hepatotoxicity via autophagy enhancement and ferroptosis inhibition.","authors":"Jingyi Ren, Ziyi Wang, Yadong Zhang, Huanting Pei, Rui Wen, Zhenao Zhang, Siqi Zhu, Xiaoya Sun, Bowen Yin, Shenghe Li, Yuxia Ma","doi":"10.1080/13510002.2025.2588863","DOIUrl":"10.1080/13510002.2025.2588863","url":null,"abstract":"Background: Acetaminophen (APAP) overdose is the leading cause of drug-induced acute liver failure. Sesamin (Ses), a natural polyphenolic compound, possesses diverse pharmacological properties. This study was to explore the effects of Ses on APAP-induced liver injury and the underlying molecular mechanism.Methods: In vivo, C57BL/6J mice were treated with different doses of Ses for 28 days. After overnight food deprivation, mice were intraperitoneally injected with a single dose of APAP. In vitro, the AML12 and HepG2 cells were pre-treated with Ses and then treated with APAP.Results: Ses dramatically alleviated APAP-induced hepatocellular injury in vitro and in vivo. Proteomic analysis suggested that the differentially expressed proteins were enriched in ferroptosis, autophagy, and FoxO signaling pathways between the APAP group and the Ses-treated groups. We subsequently found that ferroptosis was significantly inhibited, and autophagy was significantly enhanced in the Ses-treated group. Consistently, Ses obviously reduced the expression of Foxo1. However, hepatocyte-specific knockout Foxo1 abolished the effect of Ses on hepatocyte autophagy and ferroptosis caused by APAP in mice.Conclusions: Our findings demonstrate that Ses attenuates APAP-induced hepatotoxicity through Foxo1, which mediates both the activation of autophagy and the inhibition of ferroptosis. It provides a new strategy for the prevention and treatment of drug-induced liver injury.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2588863"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12632232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145550291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cytochrome P450 (CYP) 1 enzymes in acute lung injury: from molecular insights to therapeutic implications. 细胞色素P450 (CYP) 1酶在急性肺损伤中的作用：从分子观察到治疗意义

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-09-02 DOI: 10.1080/13510002.2025.2550807

Yiting You, Jingqian Huang, Xiaoyan Zhu, Hui Sheng, Yujian Liu

{"title":"Cytochrome P450 (CYP) 1 enzymes in acute lung injury: from molecular insights to therapeutic implications.","authors":"Yiting You, Jingqian Huang, Xiaoyan Zhu, Hui Sheng, Yujian Liu","doi":"10.1080/13510002.2025.2550807","DOIUrl":"10.1080/13510002.2025.2550807","url":null,"abstract":"Objective: This review aims to explore the roles and mechanisms of cytochrome P450 subfamily 1 (CYP1) enzymes in acute lung injury (ALI), and to discuss their potential as therapeutic targets.Methods: A comprehensive literature search was conducted using PubMed and Web of Science to identify relevant studies on the involvement of CYP1 enzymes-specifically CYP1A and CYP1B1-in various forms of ALI, including hyperoxic lung injury, sepsis-associated ALI, and COVID-19 pneumonia.Results: CYP1 enzymes, induced by the aromatic hydrocarbon receptor (AhR), contribute differentially to ALI. CYP1A enzymes exhibit protective effects, whereas CYP1B1 promotes lung injury, potentially through oxidative stress-related pathways such as Nrf2, NF-κB, and MAPK signaling.Conclusion: The distinct functions of CYP1 isoforms in ALI suggest their clinical relevance, highlighting the potential for isoform-specific targeting in the treatment of acute respiratory conditions.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2550807"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12406335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury. M6a去甲基化酶FTO在心肌缺血再灌注损伤中调控心肌细胞氧化应激、线粒体生物发生和PGC-1a稳定性。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-01-27 DOI: 10.1080/13510002.2025.2454892

Qiong Jiang, Xuehai Chen, Kezeng Gong, Zhe Xu, Lianglong Chen, Feilong Zhang

{"title":"M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.","authors":"Qiong Jiang, Xuehai Chen, Kezeng Gong, Zhe Xu, Lianglong Chen, Feilong Zhang","doi":"10.1080/13510002.2025.2454892","DOIUrl":"10.1080/13510002.2025.2454892","url":null,"abstract":"Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model. RT-PCR and Western blot were used to investigate the expression of the fat mass and obesity-associated (FTO) gene. Electrocardiogram, echocardiography, triphenyltetrazolium chloride (TTC) staining and hematoxylin-eosin (HE) staining were used to assess the model and the effect of FTO overexpression. The generation of reactive oxygen species (ROS) and the levels of superoxide dismutase (SOD2), mitochondrial transcription factor (TFAM) and cytochrome c oxidase I (COXI) were detected to assess the oxidative stress and mitochondrial biogenesis. RNA immunoprecipitation (RIP) and RNA pulldown assays were used to identify the interaction of FTO and PGC-1a. The m6A dot blot, methylated RNA immunoprecipitation PCR (MeRIP-PCR) and RNA stability analysis were used to analyze the regulation of methylation of PGC-1a by FTO.Results: FTO was downregulated in MIRI rats and H/R induced cardiomyocytes. Overexpression of FTO inhibited ROS level and increased the expression of SOD2, TFAM and COXI in vitro and in vivo. In addition, PGC-1a was identified as a downstream target of FTO. FTO enhanced the stability of PGC-1a mRNA through removing the m6A modification.Conclusion: Our study revealed the role of FTO regulates the oxidative stress and mitochondrial biogenesis via PGC-1a in MIRI, which may provide a new approach to mitigating MIRI.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2454892"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evaluating the anti-inflammatory and antioxidant efficacy of complementary and alternative medicines (CAM) used for management of inflammatory bowel disease: a comprehensive review. 评估用于治疗炎症性肠病的补充和替代药物（CAM）的抗炎和抗氧化功效：全面综述。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-08 DOI: 10.1080/13510002.2025.2471737

Sia Shin, Siqi Chen, Kangzhe Xie, Suehad Abou Duhun, Tamara Ortiz-Cerda

{"title":"Evaluating the anti-inflammatory and antioxidant efficacy of complementary and alternative medicines (CAM) used for management of inflammatory bowel disease: a comprehensive review.","authors":"Sia Shin, Siqi Chen, Kangzhe Xie, Suehad Abou Duhun, Tamara Ortiz-Cerda","doi":"10.1080/13510002.2025.2471737","DOIUrl":"10.1080/13510002.2025.2471737","url":null,"abstract":"Inflammatory bowel disease (IBD) is a chronic autoimmune condition whose pathogenesis has not been fully elucidated, and current treatments are not definitive and often carry several side effects. The Complementary and Alternative Medicine (CAM) offers a new approach to conventional medicine. However, their clinical application and mechanisms remain limited.Objective: The aim of this review is to evaluate the anti-inflammatory, impact on microbiota and antioxidant efficacy of currently available CAM for IBD.Methods: The literature collection was obtained from Google Scholar, MEDLINE, PubMed and Web of Science (WOS). Studies in both human and animal models, published in English language between 2018 and 2024, were selected. Sixty-seven studies were included in the current review after inclusion and exclusion screening processes.Results: Mostly, studies showed significant anti-inflammatory, gut microbiota restoring, antioxidant effects of polyphenols, polysaccharides, emodin, short-chain fatty acids (SCFA; including butyrate, propionate and acetate), and probiotics although some contrasting results were noted. Current evidence shows that polyphenols exhibit the most consistent result in alleviating IBD pathophysiology, primarily due to their significant SCFA-elevating effect.Discussion: Future studies may focus on human studies, narrowing down on individual factors which may change natural product's metabolism. Further research studies are also essential to obtain therapeutic recommendations.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2471737"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sesamin protects against Acetaminophen-induced nephrotoxicity by suppressing HMOX1-mediated apoptosis and ferroptosis. 芝麻素通过抑制hmox1介导的细胞凋亡和铁凋亡来保护对乙酰氨基酚诱导的肾毒性。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-12 DOI: 10.1080/13510002.2025.2529695

Siqi Zhu, Jingyi Ren, Yadong Zhang, Xiaoya Sun, Huanting Pei, Bowen Yin, Ziyi Wang, Zhenao Zhang, Shenghe Li, Ruonan Zhang, Ziqian Zeng, Yuxia Ma

{"title":"Sesamin protects against Acetaminophen-induced nephrotoxicity by suppressing HMOX1-mediated apoptosis and ferroptosis.","authors":"Siqi Zhu, Jingyi Ren, Yadong Zhang, Xiaoya Sun, Huanting Pei, Bowen Yin, Ziyi Wang, Zhenao Zhang, Shenghe Li, Ruonan Zhang, Ziqian Zeng, Yuxia Ma","doi":"10.1080/13510002.2025.2529695","DOIUrl":"10.1080/13510002.2025.2529695","url":null,"abstract":"Background: Acetaminophen (APAP) is a widely used antipyretic and analgesic agent, and acute exposure can lead to renal injury. Sesamin (Ses) is known for its various health benefits. However, it remains unclear whether Ses exerts a protective effect against APAP-induced kidney injury.Methods: In vivo, C57BL/6 mice were pretreated with Ses and injected intraperitoneally with APAP. In vitro, human kidney proximal tubule cells 2 were pretreated with Ses, and then models of kidney injury induced by APAP were established. Kidney damage was evaluated by morphological, inflammation, oxidative stress and protein analyzes.Results: Ses significantly improved APAP-induced nephrotoxicity in vitro and in vivo models. Transcriptomic analysis revealed that the differentially expressed genes were enriched in ferroptosis and apoptosis signaling pathways, identifying heme oxygenase 1 (HMOX1) as a core protein. In the Ses-treated group, ferroptosis and apoptosis were significantly inhibited, while HMOX1 was effectively restored. In cell experiments, both the HMOX1 agonist hemin and Ses attenuated ferroptosis and apoptosis. HMOX1 inhibitor Zinc Protoporphyrin significantly eliminated the protective effect of Ses.Conclusion: Ses alleviates APAP-induced renal injury by mediating the inhibition of ferroptosis and apoptosis via HMOX1. This study provides a new strategy for the prevention and treatment of drug-induced renal injury.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2529695"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12258237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies. 耳鼻咽喉疾病中的氧化应激和活性氧：从病理生理学到靶向抗氧化治疗的见解

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-02-02 DOI: 10.1080/13510002.2025.2458942

Linghui Meng, Shengyang Liu, Jinfeng Luo, Yanyi Tu, Tao Li, Ping Li, Jinzhuang Yu, Li Shi

{"title":"Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies.","authors":"Linghui Meng, Shengyang Liu, Jinfeng Luo, Yanyi Tu, Tao Li, Ping Li, Jinzhuang Yu, Li Shi","doi":"10.1080/13510002.2025.2458942","DOIUrl":"10.1080/13510002.2025.2458942","url":null,"abstract":"Oxidative stress, characterized by an imbalance between excessive reactive oxygen species (ROS) production and impaired antioxidant defenses, is closely linked to the pathogenesis of various otorhinolaryngological disorders. Mitochondria, as the primary site of cellular energy production, play a crucial role in modulating oxidative stress. Mitochondrial dysfunction exacerbates ROS generation, leading to cellular damage and inflammatory responses. In otorhinolaryngological diseases, oxidative stress is strongly associated with conditions such as hearing loss, allergic rhinitis, and chronic sinusitis, where oxidative damage and tissue inflammation are key pathological features. Recent studies have highlighted the potential of antioxidant therapies to mitigate oxidative stress and restore homeostasis, offering promising avenues for alleviating symptoms in these diseases. However, despite the encouraging results from early-stage research, the clinical efficacy of antioxidant interventions remains to be fully established. This review provides an overview of the role of oxidative stress in otorhinolaryngological diseases and evaluates the therapeutic potential of antioxidant strategies.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2458942"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0