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Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313810/ https://www.ncbi.nlm.nih.gov/pubmed/37391404 http://dx.doi.org/10.1038/s41420-023-01516-9 |
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author | Du, Xianfeng Liu, Ting Shen, Caijie He, Bin Feng, Mingjun Liu, Jing Zhuo, Weidong Fu, Guohua Wang, Binhao Xu, Yanyan Chu, Huimin |
author_facet | Du, Xianfeng Liu, Ting Shen, Caijie He, Bin Feng, Mingjun Liu, Jing Zhuo, Weidong Fu, Guohua Wang, Binhao Xu, Yanyan Chu, Huimin |
author_sort | Du, Xianfeng |
collection | PubMed |
description | |
format | Online Article Text |
id | pubmed-10313810 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-103138102023-07-02 Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling Du, Xianfeng Liu, Ting Shen, Caijie He, Bin Feng, Mingjun Liu, Jing Zhuo, Weidong Fu, Guohua Wang, Binhao Xu, Yanyan Chu, Huimin Cell Death Discov Retraction Note Nature Publishing Group UK 2023-06-30 /pmc/articles/PMC10313810/ /pubmed/37391404 http://dx.doi.org/10.1038/s41420-023-01516-9 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Retraction Note Du, Xianfeng Liu, Ting Shen, Caijie He, Bin Feng, Mingjun Liu, Jing Zhuo, Weidong Fu, Guohua Wang, Binhao Xu, Yanyan Chu, Huimin Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling |
title | Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling |
title_full | Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling |
title_fullStr | Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling |
title_full_unstemmed | Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling |
title_short | Retraction Note: Anti-fibrotic mechanism of SPP1 knockdown in atrial fibrosis associates with inhibited mitochondrial DNA damage and TGF-β/SREBP2/PCSK9 signaling |
title_sort | retraction note: anti-fibrotic mechanism of spp1 knockdown in atrial fibrosis associates with inhibited mitochondrial dna damage and tgf-β/srebp2/pcsk9 signaling |
topic | Retraction Note |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313810/ https://www.ncbi.nlm.nih.gov/pubmed/37391404 http://dx.doi.org/10.1038/s41420-023-01516-9 |
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