Environmental Toxicology最新文献

{"title":"Astaxanthin Alleviates Lung Injury by Regulating Oxidative Stress, Inflammatory Response, P2X7 Receptor, NF-κB, Bcl-2, and Caspase-3 in LPS-Induced Endotoxemia.","authors":"Seckin Ozkanlar, Yunusemre Ozkanlar, Adem Kara, Elif Dalkilinc","doi":"10.1002/tox.24481","DOIUrl":"https://doi.org/10.1002/tox.24481","url":null,"abstract":"<p><p>Sepsis remains the leading cause of multiple-organ injury due to endotoxemia. Astaxanthin (ASTA), widely used in marine aquaculture, has an extraordinary potential for antioxidant and anti-inflammatory activity. Purinergic receptor (e.g., P2X7R) activation is a powerful signaling in the modulation of inflammation. The effect of ASTA was investigated on the regulation of oxidative stress, inflammatory response, apoptotic mediators, and P2X7R expression in the lung injury during lipopolysaccharide (LPS)-induced endotoxemia. Twenty-four rats were blocked into four groups as Control, LPS, ASTA, and LPS + ASTA. LPS was administered by intraperitoneal injection and ASTA by gavage. Blood and lung samples were taken 6 h after the administrations. The methods were ELISA, western blotting, histopathology, and immunohistochemistry. Sepsis was confirmed by the elevations of IL-1β, IL-6, IL-10, and TNF-α levels in bloodstream. Lung injury was determined by histopathological changes. There were increased P2X7R expression, malondialdehyde (MDA), IL-1β, TNF-α, nuclear factor kappa B (NF-κB), and Caspase-3 and decreased B-cell lymphoma 2 (Bcl-2) and glutathione (GSH) in the septic lung tissue (p < 0.05). ASTA treatment improved MDA, GSH, IL-1β, TNF-α, P2X7R, NF-κB, Caspase-3, and Bcl-2 levels and reduced P2X7R immunoreactivity and histological abnormalities in the lung (p < 0.05). The production of pro-inflammatory cytokines, oxidative stress, P2X7R expression, and apoptotic mediators in the lung is associated with LPS-induced endotoxemia. The ASTA administration appears to regulate the expressions of P2X7R, NF-κB, Bcl-2, and Caspase-3 improving the antioxidative and anti-inflammatory response of the lung tissue in sepsis, in vivo.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitigating PM_2.5 Induced Myocardial Metal Deposition Through Sodium Thiosulfate Resulted in Reduction of Cardiotoxicity and Physiological Recovery From Ischemia-Reperfusion via Mitochondrial Preservation.","authors":"Bhavana Sivakumar, Gino A Kurian","doi":"10.1002/tox.24473","DOIUrl":"https://doi.org/10.1002/tox.24473","url":null,"abstract":"<p><p>The cardiovascular risks linked to PM_2.5 include calcification in both vasculature and myocardial tissues, leading to structural changes and functional decline. Through the selection of a clinically proven endogenous agent, sodium thiosulfate (STS), capable of addressing PM_2.5 related cardiac abnormalities, we not only address the absence of effective solutions to mitigate PM_2.5 toxicity, but also provide evidence for the repurposing potential of STS in ameliorating PM_2.5 induced cardiac damage. Female Wistar rats were exposed to PM_2.5 (250 μg/m³) for 3 h daily for 21 days. STS was administered thrice weekly for 3 weeks during exposure after which the hearts were excised and mounted on a Langendorff apparatus for induction of ischemia-reperfusion injury (IR). STS administration improved cardiac function in PM_2.5 exposed rat hearts, accompanied by increased expression of the master regulator gene PGC1-α and increased mitochondrial mass. Moreover, STS restored bioenergetic function and balanced mitochondrial fission-fusion dynamics. The beneficial effects of STS were further evidenced by its ability to scavenge metals, thereby reducing heavy metal deposition in mitochondria and alleviating oxidative stress and inflammation. Furthermore, STS facilitated the clearance of damaged mitochondria through mitophagy. Additionally, STS activated the PI3K/AKT/GSK3ß signaling pathway, providing cardio protection against IR injury in PM_2.5-exposed hearts by preserving mitochondrial function. These results underscore the potential therapeutic benefits of STS in mitigating the adverse cardiac effects induced by PM_2.5 exposure. The translation of these findings to clinical practice holds promise for the development of targeted interventions aimed at reducing the cardiovascular toxicity associated with PM_2.5 exposure.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intervention of a Communication Between PI3K/Akt and β-Catenin by (-)-Epigallocatechin-3-Gallate Suppresses TGF-β1-Promoted Epithelial-Mesenchymal Transition and Invasive Phenotype of NSCLC Cells.","authors":"Li-Sung Hsu, Chih-Li Lin, Min-Hsiung Pan, Wei-Jen Chen","doi":"10.1002/tox.24475","DOIUrl":"https://doi.org/10.1002/tox.24475","url":null,"abstract":"<p><p>The epithelial-mesenchymal transition (EMT) assists in the acquisition of invasiveness, relapse, and resistance in non-small cell lung cancer (NSCLC) and can be caused by the signaling of transforming growth factor-β1 (TGF-β1) through Smad-mediated or Smad-independent pathways. (-)-Epigallocatechin-3-gallate (EGCG), a multifunctional cancer-preventing bioconstituent found in tea polyphenols, has been shown to repress TGF-β1-triggered EMT in the human NSCLC A549 cell line by inhibiting the activation of Smad2 and Erk1/2 or reducing the acetylation of Smad2 and Smad3. However, its impact on the Smad-independent pathway remains unclear. Here, we found that EGCG, similar to LY294002 (a specific inhibitor of phosphatidylinositol 3-kinase [PI3K]), downregulated Akt activation and restored the action of glycogen synthase kinase-3β (GSK-3β), accompanied by TGF-β1-caused changes in hallmarks of EMT such as N-cadherin, E-cadherin, vimentin, and Snail in A549 cells. EGCG inhibited β-catenin expression and its nuclear localization caused by TGF-β1, suggesting that EGCG blocks the crosstalk between the PI3K/Akt/GSK-3β route and β-catenin. Furthermore, it was shown that EGCG suppressed TGF-β1-elicited invasive phenotypes of A549 cells, including invading and migrating activities, matrix metalloproteinase-2 (MMP-2) secretion, cell adhesion, and wound healing. In summary, we suggest that EGCG inhibits the induction of EMT by TGF-β1 in NSCLC not only through a Smad-dependent pathway, but also through the regulation of the PI3K/Akt/β-catenin signaling axis.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluoride Exposure Modulates Skeletal Development and Mineralization in Zebrafish Larvae","authors":"Harsheema Ottappilakkil, Ekambaram Perumal","doi":"10.1002/tox.24474","DOIUrl":"https://doi.org/10.1002/tox.24474","url":null,"abstract":"The presence of high levels of fluoride (F) in groundwater is a major issue worldwide. Although F is essential for healthy teeth and bones, excessive exposure can cause fluorosis or F toxicity. This condition primarily affects the hard tissues due to their high F retention capacity. F accumulation alters bone formation and resorption mechanisms interfering with mineral homeostasis and eventually manifests as skeletal fluorosis. Albeit the numerous studies on skeletal fluorosis, the effect of F on developmental osteogenesis is inconclusive. In light of this, we studied the effect of F on osteogenic differentiation, bone development, and mineralization in zebrafish. Zebrafish embryos were subjected to a low (25 ppm NaF), and a moderately high (50 ppm NaF) dose, along with a control (E3 medium alone) until 7 days postfertilization (dpf). The F content in the larvae was quantified to reveal a dose‐dependent increase in the exposed groups. Alizarin Red and alkaline phosphatase (ALP) staining suggested enhanced mineralization in the F‐treated groups. Quantitative analyses of the ALP activity and hydroxyproline (Hyp) content revealed similar results. Alcian blue staining of pharyngeal cartilages showed that F exposure alters the morphology of the major cartilages, indicating a possible craniofacial defect. Moreover, gene expression analyses of the bone markers associated with osteogenic differentiation, early mineralization, and remodeling (<jats:italic>runx2a/b</jats:italic>, <jats:italic>bmp4</jats:italic>, <jats:italic>ocn</jats:italic>, <jats:italic>osx</jats:italic>, <jats:italic>col1a1</jats:italic>, <jats:italic>alp</jats:italic>, <jats:italic>rank</jats:italic>, <jats:italic>rankl</jats:italic>, and <jats:italic>opg</jats:italic>) showed enhanced expression in the low F group. While the 50 ppm F group showed a decline in osteogenic activity, a considerable increase in the expression of mineralization markers was observed. The expression levels of cartilage markers <jats:italic>sox9a</jats:italic> and <jats:italic>sox9b</jats:italic>, remained insignificant, indicating the effect of F toxicity on osteogenesis and mineralization. Also, F exposure interferes with bone metabolism through altered osteogenic differentiation, development, and mineralization in zebrafish larvae.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"111 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143035017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Poly (Lactic‐Co‐Glycolic Acid)‐Encapsulated Endostar‐Loaded Calcium Phosphate Cement as Anti‐Tumor Bone Cement for the Treatment of Bone Metastasis in Lung Cancer","authors":"","doi":"10.1002/tox.24482","DOIUrl":"https://doi.org/10.1002/tox.24482","url":null,"abstract":"<jats:mixed-citation publication-type=\"journal\">RETRACTION: <jats:string-name><jats:given-names>Q. H.</jats:given-names> <jats:surname>Tian</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>C.</jats:given-names> <jats:surname>Tian</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>Y. Y.</jats:given-names> <jats:surname>Lu</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>B. C.</jats:given-names> <jats:surname>Yan</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>K.</jats:given-names> <jats:surname>Zhang</jats:surname></jats:string-name>, and <jats:string-name><jats:given-names>C. G.</jats:given-names> <jats:surname>Wu</jats:surname></jats:string-name>, “,” <jats:source>Environmental Toxicology</jats:source> (EarlyView): <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.24166\">https://doi.org/10.1002/tox.24166</jats:ext-link>.</jats:mixed-citation>The above article, published online on 23 February 2024, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Paul B. Tchounwou; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"10 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: The Role of PKP1 in Tumor Progression in Melanoma: Analysis of a Cell Adhesion‐Related Model","authors":"","doi":"10.1002/tox.24483","DOIUrl":"https://doi.org/10.1002/tox.24483","url":null,"abstract":"<jats:mixed-citation publication-type=\"journal\">RETRACTION: <jats:string-name><jats:given-names>C.</jats:given-names> <jats:surname>Yue</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>W.</jats:given-names> <jats:surname>Lian</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>Z.</jats:given-names> <jats:surname>Fan</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>H.</jats:given-names> <jats:surname>Li</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>M.</jats:given-names> <jats:surname>Duan</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>L.</jats:given-names> <jats:surname>Qin</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>X.</jats:given-names> <jats:surname>Cao</jats:surname></jats:string-name>, and <jats:string-name><jats:given-names>J.</jats:given-names> <jats:surname>Peng</jats:surname></jats:string-name>, “,” <jats:source>Environmental Toxicology</jats:source> <jats:volume>39</jats:volume>, no. (<jats:year>2024</jats:year>): <jats:fpage>915</jats:fpage>–<jats:lpage>926</jats:lpage>, <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.24017\">https://doi.org/10.1002/tox.24017</jats:ext-link>.</jats:mixed-citation>The above article, published online on 15 November 2023, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Paul B. Tchounwou; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. The authors agree with this decision.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"6 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Calcitriol Suppresses Gastric Cancer Progression and Cisplatin Resistance by Inhibiting Glycolysis and M2 Macrophage Polarization Through Inhibition of mTOR Activation","authors":"","doi":"10.1002/tox.24484","DOIUrl":"https://doi.org/10.1002/tox.24484","url":null,"abstract":"<jats:mixed-citation publication-type=\"journal\">RETRACTION: <jats:string-name><jats:given-names>L.</jats:given-names> <jats:surname>Jie</jats:surname></jats:string-name>, <jats:string-name><jats:given-names>W.</jats:given-names> <jats:surname>Hengyue</jats:surname></jats:string-name>, and <jats:string-name><jats:given-names>H.</jats:given-names> <jats:surname>Ting</jats:surname></jats:string-name>, “,” <jats:source>Environmental Toxicology</jats:source> <jats:volume>39</jats:volume>, no. (<jats:year>2024</jats:year>): <jats:fpage>830</jats:fpage>–<jats:lpage>839</jats:lpage>, <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.23975\">https://doi.org/10.1002/tox.23975</jats:ext-link></jats:mixed-citation>The above article, published online on 4 October 2023, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Paul B. Tchounwou; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"61 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Environmentally Relevant Concentrations of Roundup on Oxidative‐Nitrative Stress, Cellular Apoptosis, Prooxidant‐Antioxidant Homeostasis, Renin and CYP1A Expressions in Goldfish: Molecular Mechanisms Underlying Kidney Damage During Roundup Exposure","authors":"Md Imran Noor, Md Saydur Rahman","doi":"10.1002/tox.24471","DOIUrl":"https://doi.org/10.1002/tox.24471","url":null,"abstract":"Roundup is one of the most widely used glyphosate‐based harmful herbicides in the United States as well as globally, which poses a severe risk for terrestrial and aquatic organisms. In order to identify the detrimental effects of Roundup exposure in aquatic organisms, we investigated the environmentally relevant concentrations of Roundup exposure (low dose: 0.5 μg/L and high dose: 5.0 μg/L for 2 weeks) on renin expression, oxidative‐nitrative stress biomarkers (e.g., 2,4‐dinitrophenol, DNP; and 3‐nitrotyrosine protein, NTP), prooxidant‐antioxidant enzymes expressions (e.g., superoxide dismutase, SOD; and catalase, CAT), cellular apoptosis, and cytochrome P450 1A (CYP1A) mRNA levels in the kidneys of goldfish (<jats:styled-content style=\"fixed-case\"><jats:italic>Carassius auratus</jats:italic></jats:styled-content>). Histopathological and in situ TUNEL analyses showed widespread tissue disruption (e.g., bowman's capsule shrinkage, melanin pigment formation, etc.) and induced apoptotic nuclei in the kidneys of goldfish. Immunohistochemical and quantitative real‐time PCR (qRT‐PCR) analyses showed a significant (<jats:italic>p</jats:italic> &lt; 0.05) increase in the expression of renin, DNP, NTP, SOD, and CAT, as well as CYP1A mRNA levels in the kidneys of fish exposed to Roundup. These results suggest that environmentally relevant concentrations of Roundup disrupt kidney architecture by inducing oxidative‐nitrative stress, cellular apoptosis, and change in osmoregulatory enzymes (i.e., renin) and prooxidant‐antioxidant systems in the kidneys of teleost fishes.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"49 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: DNMT1‐Mediated Regulating on FBXO32 Promotes the Progression of Glioma Cells Through the Regulation of SKP1 Activity","authors":"","doi":"10.1002/tox.24485","DOIUrl":"https://doi.org/10.1002/tox.24485","url":null,"abstract":"<jats:mixed-citation publication-type=\"journal\">RETRACTION: <jats:string-name><jats:given-names>J.</jats:given-names> <jats:surname>Quan</jats:surname></jats:string-name> and <jats:string-name><jats:given-names>C.</jats:given-names> <jats:surname>Ma</jats:surname></jats:string-name>, “,” <jats:source>Environmental Toxicology</jats:source> <jats:volume>39</jats:volume>, no. (<jats:year>2024</jats:year>): <jats:fpage>783</jats:fpage>–<jats:lpage>793</jats:lpage>, <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.23976\">https://doi.org/10.1002/tox.23976</jats:ext-link>.</jats:mixed-citation>The above article, published online on 2 October 2023, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Paul B. Tchounwou; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"58 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Refining Molecular Subtypes and Risk Stratification of Ovarian Cancer Through Multi-Omics Consensus Portfolio and Machine Learning.","authors":"","doi":"10.1002/tox.24479","DOIUrl":"https://doi.org/10.1002/tox.24479","url":null,"abstract":"<p><strong>Retraction: </strong>J. Zhang, S. He, and H. Ying, \"Refining Molecular Subtypes and Risk Stratification of Ovarian Cancer Through Multi-Omics Consensus Portfolio and Machine Learning,\" Environmental Toxicology (EarlyView): https://doi.org/10.1002/tox.24222. The above article, published online on 13 March 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}