撤回到“脂肪组织来源的干细胞通过p38/MAPK途径抑制肥厚性瘢痕（HS）纤维化”。

IF 3 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of cellular biochemistry Pub Date : 2024-12-10 DOI:10.1002/jcb.30689

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引用次数: 0

摘要

收缩:彭译葶。柴俊，宋志强，谭志强。张春华，孙淑娟，“脂肪组织源性干细胞抑制增生性瘢痕（HS）纤维化的研究进展”，《细胞生物化学杂志》，第12期。3 (2019): 4057-4064, https://doi.org/10.1002/jcb.27689。上述文章于2018年9月27日在线发表在Wiley在线图书馆（wileyonlinelibrary.com）上，经作者同意撤回；杂志主编克里斯蒂安·贝尔；和Wiley期刊有限责任公司。由于第三方对文章中提供的数据提出了担忧，已经同意撤回。具体来说，图1、2、3和4中的多个图像元素被发现是由不同的作者小组先前发表过的。因此，本文的结论被编辑认为是无效的。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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RETRACTION to “Adipose Tissue-Derived Stem Cells Inhibit Hypertrophic Scar (HS) Fibrosis via p38/MAPK Pathway”

RETRACTION: C.-Y. Chai, J. Song, Z. Tan, I.-C. Tai, C. Zhang, and S. Sun, “Adipose Tissue-Derived Stem Cells Inhibit Hypertrophic Scar (HS) Fibrosis via p38/MAPK Pathway,” Journal of Cellular Biochemistry 120, no. 3 (2019): 4057–4064, https://doi.org/10.1002/jcb.27689.

The above article, published online on 27 September 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, multiple image elements in Figures 1, 2, 3, and 4 were found to have been previously published by different author groups. Accordingly, the conclusions of this article are considered invalid by the editors.

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来源期刊

Journal of cellular biochemistry 生物-生化与分子生物学

CiteScore

9.90

自引率

0.00%

发文量

164

审稿时长

1 months

期刊介绍： The Journal of Cellular Biochemistry publishes descriptions of original research in which complex cellular, pathogenic, clinical, or animal model systems are studied by biochemical, molecular, genetic, epigenetic or quantitative ultrastructural approaches. Submission of papers reporting genomic, proteomic, bioinformatics and systems biology approaches to identify and characterize parameters of biological control in a cellular context are encouraged. The areas covered include, but are not restricted to, conditions, agents, regulatory networks, or differentiation states that influence structure, cell cycle & growth control, structure-function relationships.