After this article [1] was published, concerns were raised regarding results presented in Figs 1, and 3-6.
Specifically:
- The following lanes appear similar despite representing different experimental conditions:
- ◦. Fig 3D ATG9A lane 1 and Fig 5D ATG9A lane 3
- ◦. Fig 4D GAPDH lane 2 and Fig 4D GAPDH lane 3 flipped horizontally
- ◦. Fig 4D GAPDH lane 1 and Fig 5C GAPDH lane 2
- In the Fig 5C Con AngII p62 panel there appears to be a vertical discontinuity in the background between lanes 1 and 2.
- The Fig 1B Sham and TAAC panels of [1] appear similar to Figs 7A and 7E of [2] respectively.
- The following results appear similar despite representing different experimental conditions:
The authors did not respond to editorial requests for a response and underlying data. In light of the above unresolved concerns that question the integrity and reliability of the reported results and conclusions, the PLOS One Editors retract this article.
All authors either did not respond directly or could not be reached.
References
- 1. Huang J, Sun W, Huang H, Ye J, Pan W, Zhong Y, et al. miR-34a modulates angiotensin II-Induced myocardial hypertrophy by direct inhibition of ATG9A expression and autophagic activity. PLoS One. 2014;9(4):e94382. pmid:24728149
- 2. Dai W, Dong Q, Chen M, Zhao L, Chen A, Li Z, et al. Changes in cardiac structure and function in a modified rat model of myocardial hypertrophy. Cardiovasc J Afr. 2016;27(3):134–42. pmid:27841899
- 3. Huang J, Huang H, Pan W, Ou D, Dai W, Lin Y, et al. Renal denervation attenuates cardiac hypertrophy in spontaneously hypertensive rats via regulation of autophagy. Mol Med Rep. 2017;16(2):2023–9. pmid:28627693
Citation: The PLOS One Editors (2025) Retraction: miR-34a modulates Angiotensin II-induced myocardial hypertrophy by direct inhibition of ATG9A expression and Autophagic activity. PLoS ONE 20(2): e0319360. https://doi.org/10.1371/journal.pone.0319360
Published: February 19, 2025
Copyright: © 2025 The PLOS ONE Editors.. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.