Redox Report最新文献

{"title":"WTAP-mediated m⁶A modification of TRIM22 promotes diabetic nephropathy by inducing mitochondrial dysfunction via ubiquitination of OPA1.","authors":"Zeng Zhang, Fengzhu Zhou, Min Lu, Duanchun Zhang, Xinyi Zhang, Siyu Xu, Yanming He","doi":"10.1080/13510002.2024.2404794","DOIUrl":"10.1080/13510002.2024.2404794","url":null,"abstract":"<p><strong>Objectives: </strong>Diabetic nephropathy (DN) is one of the most serious microvascular complications of diabetes and is the most common cause of end-stage renal disease. Tripartite motif-containing (TRIM) proteins are a large family of E3 ubiquitin ligases that contribute to protein quality control by regulating the ubiquitin - proteasome system. However, the detailed mechanisms through which various TRIM proteins regulate downstream events have not yet been fully elucidated. The current research aimed to determine the function and mechanism of TRIM22 in DN.</p><p><strong>Methods: </strong>DN models were established by inducing HK-2 cells using high glucose (HG) and diabetic mice (db/db mice). Cell viability, apoptosis, mitochondrial reactive oxygen species, and mitochondrial membrane potential were detected by Cell Counting Kit-8 and flow cytometry, respectively. Pathological changes were evaluated using hematoxylin and eosin, periodic acid schiff and Masson staining. The binding between TRIM22 and optic atrophy 1 (OPA1) was analyzed using co-immunoprecipitation. The m⁶A level of TRIM22 5'UTR was detected using RNA immunoprecipitation.</p><p><strong>Results: </strong>TRIM22 was highly expressed in patients with DN. TRIM22 silencing inhibited HG-induced apoptosis and mitochondrial dysfunction in HK-2 cells. Promoting mitochondrial fusion alleviated TRIM22 overexpression-induced cell apoptosis, mitochondrial dysfunction in HK-2 cells, and kidney damage in mice. Mechanistically, TRIM22 interacted with OPA1 and induced its ubiquitination. Wilms tumor 1-associating protein (WTAP) promoted m⁶A modification of TRIM22 through the m⁶A reader insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1).</p><p><strong>Discussion: </strong>TRIM22 silencing inhibited the progression of DN by interacting with OPA1 and inducing its ubiquitination. Furthermore, WTAP promoted m⁶A modification of TRIM22 via IGF2BP1.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2404794"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11423538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308523","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}

{"title":"Hesperidin activates Nrf2 to protect cochlear hair cells from cisplatin-induced damage","authors":"Jintao Lou, Fan Wu, Wuhui He, Rui Hu, Ziyi Cai, Guisheng Chen, Wenji Zhao, Zhigang Zhang, Yu Si","doi":"10.1080/13510002.2024.2341470","DOIUrl":"https://doi.org/10.1080/13510002.2024.2341470","url":null,"abstract":"Cisplatin is widely employed in clinical oncology as an anticancer chemotherapy drug in clinical practice and is known for its severe ototoxic side effects. Prior research indicates that the accumu...","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140608768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc ameliorates acrylamide-induced oxidative stress and apoptosis in testicular cells via Nrf2/HO-1/NfkB and Bax/Bcl2 signaling pathway","authors":"Ayodeji Johnson Ajibare, Adeyemi Fatai Odetayo, Olabode Oluwadare Akintoye, Luqman Aribidesi Olayaki","doi":"10.1080/13510002.2024.2341537","DOIUrl":"https://doi.org/10.1080/13510002.2024.2341537","url":null,"abstract":"Acrylamide is a toxic substance formed in some foods that require high-temperature cooking processes and has been implicated as a gonadotoxic agent. Zinc, on the other hand, is a known antioxidant ...","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"12 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140617781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astaxanthin prevents bone loss in osteoporotic rats with palmitic acid through suppressing oxidative stress","authors":"Zhou-Shan Tao, Xing-Jing Wu, Min Yang, Cai-Liang Shen","doi":"10.1080/13510002.2024.2333096","DOIUrl":"https://doi.org/10.1080/13510002.2024.2333096","url":null,"abstract":"The study aimed to assess the role of Astaxanthin (ATX) in palmitic acid(PA) -induced bone loss in Ovariectomized(OVX) rats.In the OVX rat model, we observed that PA affects bone metabolism and acc...","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140586617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing the bioavailability and activity of natural antioxidants with nanobubbles and nanoparticles","authors":"Miroslav Čolić, Sandra Kraljević Pavelić, Željka Peršurić, Andrea Agaj, Aleksandar Bulog, Krešimir Pavelić","doi":"10.1080/13510002.2024.2333619","DOIUrl":"https://doi.org/10.1080/13510002.2024.2333619","url":null,"abstract":"Objectives: Many polyphenols such as EGCG from green tea, curcumin, apigenin, resveratrol or the alkaloid berberine show in-vitro activity that is much higher than FDA and EU approved drugs. And ye...","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140586482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation","authors":"Yanmin Jiang, Lan Xu, Xue Zhu, Xiaowei Zhu, Xiang Xu, Jianbo Li","doi":"10.1080/13510002.2024.2324234","DOIUrl":"https://doi.org/10.1080/13510002.2024.2324234","url":null,"abstract":"Diabetic gastrointestinal dysfunction (DGD) is a serious complication of diabetic mellitus (DM), affecting the enteric nervous system (ENS), particular enteric glial cells (EGCs). This study aimed ...","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"37 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140036801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated approach to reducing polypharmacy in older people: exploring the role of oxidative stress and antioxidant potential therapy","authors":"Catalina Rojas-Solé, Víctor Pinilla-González, José Lillo-Moya, Tommy González-Fernández, Luciano Saso, Ramón Rodrigo","doi":"10.1080/13510002.2023.2289740","DOIUrl":"https://doi.org/10.1080/13510002.2023.2289740","url":null,"abstract":"Increased life expectancy, attributed to improved access to healthcare and drug development, has led to an increase in multimorbidity, a key contributor to polypharmacy. Polypharmacy is characteris...","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"15 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138715058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obstructive sleep apnea promotes the progression of lung cancer by modulating cancer cell invasion and cancer-associated fibroblast activation via TGFβ signaling.","authors":"Zhilei Cui, Zhengshang Ruan, Meigui Li, Rongrong Ren, Yizong Ma, Junxiang Zeng, Jinyuan Sun, Wenjing Ye, Weiguo Xu, Xuejun Guo, Dengfei Xu, Linlin Zhang","doi":"10.1080/13510002.2023.2279813","DOIUrl":"10.1080/13510002.2023.2279813","url":null,"abstract":"<p><strong>Objective: </strong>Obstructive sleep apnea (OSA) is associated with severity of pneumonia; however, the mechanism by which OSA promotes lung cancer progression is unclear.</p><p><strong>Methods: </strong>Twenty-five lung cancer patients were recruited to investigate the relationship between OSA and cancer-associated fibroblast (CAFs) activation. Lung cancer cells (A549) and WI38 fibroblast cells were used to explore the hypoxia-induced TGFβ expression using qPCR, Western blot, and ELISA. Wound healing and transwell assays were performed to evaluate cancer cell migration and invasion. A549 or A549-Luc + WI38 xenograft mouse models were established to detect the intermittent hypoxia (IH) associated with lung tumor growth and epithelial-mesenchymal transition (EMT) <i>in vivo</i>.</p><p><strong>Results: </strong>OSA promotes CAF activation and enrichment in lung cancer patients. Hypoxia (OSA-like treatment) activated TGFβ signaling in both lung cancer cells and fibroblasts, which promoted cancer cell migration and invasion, and enriched CAFs. IH promoted the progression and EMT process of lung cancer xenograft tumor. Co-inoculation of lung cancer cells and fibroblast cells could further promote lung cancer progression.</p><p><strong>Conclusions: </strong>IH promotes lung cancer progression by upregulating TGFβ signaling, promoting lung cancer cell migration, and increasing the CAF activation and proportion of lung tumors.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"28 1","pages":"2279813"},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138446072","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}

{"title":"Evaluation of oxidative stress level: reactive oxygen species, reduced glutathione, and D-dimer in patients hospitalized due to COVID-19.","authors":"Claudionei Roessler, Karen Cristine Silva de Oliveira, Auricélia Xavier de Oliveira Portella, Paulo Cezar Nunes Fortes, Franciéle Romero Machado, Stífani Machado Araujo, Marina Prigol, Léia Carolina Lucio, Dalila Moter Benvegnú, Lirane Elize Defante Ferreto","doi":"10.1080/13510002.2023.2272384","DOIUrl":"10.1080/13510002.2023.2272384","url":null,"abstract":"<p><p>Elevated D-dimer levels at hospital admission may also indicate a higher likelihood of progressing to a severe or critical state. This study aimed to assess reactive oxygen species (ROS), non-enzymatic antioxidant reduced glutathione (GSH), and D-dimer levels in COVID-19 patients upon admission, examining their association with mortality outcomes. Data was collected from the medical records of 170 patients hospitalized in a referral hospital unit between March 2020 and December 2021. Patients were divided into two groups: the ward bed group (<i>n</i> = 87), comprising 51% with moderate clinical conditions, and the intensive care unit (ICU) group (<i>n</i> = 83), comprising 49% with severe conditions. The mean age was 59.4 years, with a male predominance of 52.4%. The overall death rate was 43%, with 30.6% in the moderate group and 69.4% in the severe group. The average time from symptom onset to hospitalization was 6.42 days. Results showed that non-survivors had high D-dimer and ROS counts, longer ICU stays, and worse saturation levels at admission. In conclusion, elevated ROS and D-dimer levels may contribute to worse outcomes in critically ill patients, potentially serving as specific and sensitive predictors of poor outcomes upon admission.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"28 1","pages":"1-6"},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470753","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}

{"title":"Melittin kills A549 cells by targeting mitochondria and blocking mitophagy flux.","authors":"Xuan Li, Zheng Li, Yu-Qi Meng, Hui Qiao, Ke-Rong Zhai, Zhen-Qing Li, Shi-Lin Wei, Bin Li","doi":"10.1080/13510002.2023.2284517","DOIUrl":"10.1080/13510002.2023.2284517","url":null,"abstract":"<p><p>Melittin, a naturally occurring polypeptide found in bee venom, has been recognized for its potential anti-tumor effects, particularly in the context of lung cancer. Our previous study focused on its impact on human lung adenocarcinoma cells A549, revealing that melittin induces intracellular reactive oxygen species (ROS) burst and oxidative damage, resulting in cell death. Considering the significant role of mitochondria in maintaining intracellular redox levels and ROS, we further examined the involvement of mitochondrial damage in melittin-induced apoptosis in lung cancer cells. Our findings demonstrated that melittin caused changes in mitochondrial membrane potential (MMP), triggered mitochondrial ROS burst (Figure 1), and activated the mitochondria-related apoptosis pathway Bax/Bcl-2 by directly targeting mitochondria in A549 cells (Figure 2). Further, we infected A549 cells using a lentivirus that can express melittin-Myc and confirmed that melittin can directly target binding to mitochondria, causing the biological effects described above (Figure 2). Notably, melittin induced mitochondrial damage while inhibiting autophagy, resulting in abnormal degradation of damaged mitochondria (Figure 5). To summarize, our study unveils that melittin targets mitochondria, causing mitochondrial damage, and inhibits the autophagy-lysosomal degradation pathway. This process triggers mitoROS burst and ultimately activates the mitochondria-associated Bax/Bcl-2 apoptotic signaling pathways in A549 cells.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"28 1","pages":"2284517"},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470754","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}