RETRACTION: LncRNA SNHG1 Regulates Cerebrovascular Pathologies as a Competing Endogenous RNA Through HIF-1α/VEGF Signaling in Ischemic Stroke

IF 3 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of cellular biochemistry Pub Date : 2025-04-03 DOI:10.1002/jcb.70017

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引用次数: 0

Abstract

RETRACTION: L. Zhang, X. Luo, F. Chen, W. Yuan, X. Xiao, X. Zhang, Y. Dong, Y. Zhang, and Y. Liu, “LncRNA SNHG1 Regulates Cerebrovascular Pathologies as a Competing Endogenous RNA Through HIF-1α/VEGF Signaling in Ischemic Stroke, ” Journal of Cellular Biochemistry 119, no. 7 (2018): 5460-5472, https://doi.org/10.1002/jcb.26705.

The above article, published online on 27 January 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Image elements within Figures 3 C and 6 F were found to have been published previously by different authors in different scientific contexts. The authors were invited to comment on these concerns but did not respond. Accordingly, the article is retracted as the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider its conclusions invalid. The authors were informed of the retraction.

查看原文本刊更多论文

在缺血性卒中中，LncRNA SNHG1作为竞争内源性RNA通过HIF-1α/VEGF信号通路调控脑血管病理

引用本文：张莉，罗晓霞，陈峰，袁伟，肖晓霞，张晓霞，董艳，张艳，刘艳，“LncRNA SNHG1作为竞争内源性RNA通过HIF-1α/VEGF信号通路调控缺血性脑卒中的脑血管病，细胞生物化学119，no。7 (2018): 5460-5472, https://doi.org/10.1002/jcb.26705.The上述文章于2018年1月27日在线发表在Wiley online Library （wileyonlinelibrary.com）上，经主编Christian Behl同意撤回；和Wiley期刊有限责任公司。由于第三方提出的担忧，已同意撤回。图3c和图6f中的图像元素被发现以前由不同的作者在不同的科学背景下发表过。作者被邀请对这些担忧发表评论，但没有回应。因此，由于编辑对文章中提供的全部数据的完整性和可靠性失去信心，并认为其结论无效，因此文章被撤回。作者被告知撤稿。

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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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.