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CORRECTION article

Front. Cell Dev. Biol., 25 July 2024

Sec. Stem Cell Research

Volume 12 - 2024 | https://doi.org/10.3389/fcell.2024.1419893

Corrigendum: Nitric oxide alleviated high salt-induced cardiomyocyte apoptosis and autophagy independent of blood pressure in rats

    YL

    Yong Li 1

    XW

    Xiaoguang Wu 1

    YM

    Yukang Mao 1

    CL

    Chi Liu 2

    YW

    Yiting Wu 3

    JT

    Junzhe Tang 3

    KZ

    Kun Zhao 1*

    PL

    Peng Li 1*

  • 1. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China

  • 2. Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China

  • 3. The First School of Clinical Medicine, Nanjing Medical University, Nanjing, China

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In the published article, there was an error in Figure 5J as published. The wrong representative image of TUNEL-staining was used. The corrected Figure 5 and its caption appear below.

FIGURE 5

FIGURE 5

Effects of different doses of nitric oxide donor sodium nitroprusside (SNP) on NaCl-induced apoptosis and autophagy in H9C2 cells. (A–I), SNP attenuated the increases in the levels of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and autophagy related 7 (ATG7), and enhanced the decrease of p-endothelial nitric oxide synthase (eNOS) induced by NaCl (100 mM) in H9C2 cells. (J) The increase of TUNEL-positive cell number was inhibited by high dose of SNP (100 µM), but not middle (10 µM) or low dose (1 µM) of SNP. The results are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

In the published article, there was an error in Figure 7J as published. The wrong representative image of TUNEL-staining was used. The corrected Figure 7 and its caption appear below.

FIGURE 7

FIGURE 7

Effects of nitric oxide donor sodium nitroprusside (SNP) on apoptosis and autophagy induced by three doses of sodium chloride (NaCl) in primary neonatal rat cardiomyocytes (NRCM). SNP (100 µM) attenuated the increases in the levels of cleaved-caspase 3/caspase 3 (A, B), cleaved-caspase 8/caspase 8 (A, C), Bax/Bcl2 (A, D), LC3 II/LC3 I (A,E), Beclin-1 (H), and autophagy related 7 (ATG7) (I), and enhanced the decrease of p-endothelial nitric oxide synthase (eNOS) induced by NaCl (50 or 100 mM) in NRCM (F, G). The increases of TUNEL-positive cell numbers induced by three doses of NaCl in the NRCM were attenuated by SNP (100 µM) treatment (J). The results are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

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

high-salt diet, cardiomyocytes, apoptosis, autophagy, nitric oxide, sodium nitroprusside

Citation

Li Y, Wu X, Mao Y, Liu C, Wu Y, Tang J, Zhao K and Li P (2024) Corrigendum: Nitric oxide alleviated high salt-induced cardiomyocyte apoptosis and autophagy independent of blood pressure in rats. Front. Cell Dev. Biol. 12:1419893. doi: 10.3389/fcell.2024.1419893

Received

19 April 2024

Accepted

15 July 2024

Published

25 July 2024

Volume

12 - 2024

Edited and reviewed by

Valerie Kouskoff, The University of Manchester, United Kingdom

Updates

Copyright

*Correspondence: Peng Li, ; Kun Zhao,

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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