CORRECTION article

Front. Cardiovasc. Med., 08 August 2025

Sec. Cardiovascular Metabolism

Volume 12 - 2025 | https://doi.org/10.3389/fcvm.2025.1578594

Corrigendum: The cardiac dysfunction caused by metabolic alterations in Alzheimer's disease

  • 1. Department of Surgery, Morsani College of Medicine, University of South Florida, Tampa, FL, United States

  • 2. Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, United States

  • 3. Cardiology Section, Medical Service, Richmond Department of Veterans Affairs Medical Center, Richmond, VA, United States

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In the published article, there was an error in the legend for Figure 2A and 2B as published. In Figure 2A the data represents contractility measurements from isolated cardiomyocytes, not from whole heart tissue, the reported number of biological replicates did not accurately reflect the number of individual cardiomyocytes analyzed per group. In Figure 2B the data represents calcium flux measurements from isolated cardiomyocytes, not from whole heart tissue, the reported number of biological replicates did not accurately reflect the number of individual cardiomyocytes analyzed per group. The corrected legend appears below.

Figure 2. Cardiomyocytes of 5XFAD mice exhibited impaired extend and rate of contraction associated with decreased calcium influx, (A) The contractile properties of isolated cardiomyocytes from 5XFAD (6 months) and WT (6 months) hearts. Biological replicates N = 47–68 for each group, these cardiomyocytes were isolated from a total of six mice. P-value determined by two-tailed students t-test. (B) The transient calcium signal response of the isolated cardiomyocytes from 5XFAD (6 months) and WT (6 months) hearts. Biological replicates N = 24–40 for each group, these cardiomyocytes were isolated from a total of six mice. P-value determined by two-tailed students t-test. (C) Immunoblotting showed the phosphorylation of AMPK at Threonine 172 in left ventricles from 5XFAD (6 months) and WT (6 months) hearts. Biological replicates N = 6 for each group. P-value determined by two-tailed students t-test. (D) Immunoblotting showed the phosphorylation of AMPK at Threonine 172 in the hippocampus and cortex from 5XFAD (6 months) and WT (6 months). Biological replicates N = 6 for each group. P-value determined by two-tailed students t-test.

In the published article, there was an error in Figure 1B as published. The data in R amplitude represents both technical replicates and biological replicates. Therefore, there are more datapoints than the reported number of biological replicates N = 8 per group. The PR interval in Figure 1B was inadvertently duplicated in the final manuscript. This error appears to have been introduced during the final proof submission due to a technical issue when transferring files via different system. The corrected Figure 1 and its caption appear below.

Figure 1

Figure 3

Figure 4

Figure 5

In the published article, there was an error in Figure 3A, 3B and 3C as published. In Figure 3A the data in Basal Respiration and Maximal Respiration represent both biological dependent replicates (Left ventricular tissues) and biological independent replicates (different mice). Therefore, there are more datapoints than the reported number of biological replicates N = 6 per group. In Figure 3B the data in Basal Respiration and Maximal Respiration represent both biological dependent replicates (Hippocampus tissues) and biological independent replicates (different mice). Therefore, there are more datapoints than the reported number of biological replicates N = 6 per group. In Figure 3C Ctx OCR was inadvertently duplicated. The data in Basal Respiration and Maximal Respiration represent both biological dependent replicates (Cortex tissues) and biological independent replicates (different mice). Therefore, there are more datapoints than the reported number of biological replicates N = 6 per group. The corrected Figure 3 and its caption appear below.

In the published article, there was an error in Figure 4A and 4B as published. The data in left ventricular, hippocampus, and cortex represent both biological dependent replicates (multiple imaging sections) and biological independent replicates (different mice). Therefore, there are more datapoints than the reported number of biological replicates N = 3 per group. The corrected Figure 4 and its caption appear below.

In the published article, there was an error in Figure 5C as published. The data in Figure 5C represent both biological dependent replicates (multiple imaging sections) and biological independent replicates (different mice). Therefore, there are more datapoints than the reported number of biological replicates N = 3 per group. The corrected Figure 5 and its caption appear below.

The authors apologize for these errors and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

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Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Summary

Keywords

Alzheimer's Disease, cardiac dysfunction, mitochondrial deficits, metabolic regulation, glucose metabolic alterations

Citation

Murphy J, Le TNV, Fedorova J, Yang Y, Krause-Hauch M, Davitt K, Zoungrana LI, Fatmi MK, Lesnefsky EJ, Li J and Ren D (2025) Corrigendum: The cardiac dysfunction caused by metabolic alterations in Alzheimer's disease. Front. Cardiovasc. Med. 12:1578594. doi: 10.3389/fcvm.2025.1578594

Received

17 February 2025

Accepted

08 July 2025

Published

08 August 2025

Volume

12 - 2025

Edited by

Ichiro Manabe, Chiba University, Japan

Reviewed by

Ippei Shimizu, Juntendo University, Japan

Andrea Elia, Temple University, United States

Updates

Copyright

*Correspondence: Di Ren

†These authors have contributed equally to this work

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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