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      Retracted: Dapagliflozin Improves Diabetic Cardiomyopathy by Modulating the Akt/mTOR Signaling Pathway

      retraction
      BioMed Research International
      Hindawi

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          Abstract

          This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation The presence of these indicators undermines our confidence in the integrity of the article's content and we cannot, therefore, vouch for its reliability. Please note that this notice is intended solely to alert readers that the content of this article is unreliable. We have not investigated whether authors were aware of or involved in the systematic manipulation of the publication process. Wiley and Hindawi regrets that the usual quality checks did not identify these issues before publication and have since put additional measures in place to safeguard research integrity. We wish to credit our own Research Integrity and Research Publishing teams and anonymous and named external researchers and research integrity experts for contributing to this investigation. The corresponding author, as the representative of all authors, has been given the opportunity to register their agreement or disagreement to this retraction. We have kept a record of any response received.

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          Dapagliflozin Improves Diabetic Cardiomyopathy by Modulating the Akt/mTOR Signaling Pathway

          Background Dapagliflozin can significantly improve heart failure, and Cx43 is one of the molecular mechanisms of heart failure. This study investigated the effect of dapagliflozin on Cx43 and Akt/mTOR signaling pathway in ventricular myocytes. Methods A rat model of type 2 diabetes mellitus was established by high-fat diet combined with streptozotocin, and the animals were treated randomly with dapagliflozin. The morphological changes of the myocardium were observed by hematoxylin eosin staining, and the expression and distribution of Cx43 in ventricular myocytes were detected by immunohistochemistry. And Western blot determined the expressions of Cx43, Akt, mTOR, p62, and LC3 proteins in rat myocardium. Results Compared with the normal control group, the heart rate of diabetic rats decreased significantly ( p < 0.05), QRS wave of ECG widened, and QT interval prolonged ( p < 0.05). Dapagliflozin treatment in diabetic rats resulted in improvements in these ECG indexes ( p < 0.05) with early administration group obtaining greater efficacy than the late administration group ( p < 0.05). In the normal control group, the cardiomyocytes were arranged orderly, and the expression of Cx43 was dense, uniform, and regular, which was higher than that in the intercalated disc. In the diabetic control model group, the cardiomyocytes were enlarged and presented disorderly with detection of Cx43 in the cytoplasm. Early use of dapagliflozin better improved these myocardial tissue lesions. Of note, as diabetic rats exhibited decreased expression of Cx43, Akt, and mTOR ( p < 0.05), increased p62 expression ( p < 0.05), and decreased LC3-II/I ratio ( p < 0.05), administration of dapagliflozin partially reversed the expression of the above proteins ( p < 0.05) with greater improvement in the early administration group compared with the late administration group ( p < 0.05). Conclusions Dapagliflozin increases the expression of Cx43 in cardiomyocytes of diabetic rats and thereby alleviates heart failure partly through regulating the Akt/mTOR signaling pathway.
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            Author and article information

            Contributors
            Journal
            Biomed Res Int
            Biomed Res Int
            BMRI
            BioMed Research International
            Hindawi
            2314-6133
            2314-6141
            2023
            21 June 2023
            21 June 2023
            : 2023
            : 9765065
            Affiliations
            Article
            10.1155/2023/9765065
            10307049
            abc78d9c-f920-49a5-b908-2f0a136f0f50
            Copyright © 2023 BioMed Research International.

            This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

            History
            : 20 June 2023
            : 20 June 2023
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            Retraction

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