Evidence map›Paper›PMID 39011065›Full record

ArticleExperimental and therapeutic medicine2024

Zinc finger translocation‑associated protein promotes ferroptosis through the upregulation of ACSL4 expression in vascular endothelial cells.

Hui-Xin Gao, Jun Jiang, Chun-Yan Yang, Jin-Fu Xu, Qing He, Yan-Wei Hu

Abstract read
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Article in Experimental and therapeutic medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Hui-Xin GaoDepartment of Clinical Laboratory, Guangzhou Women and Children Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510600, P.R. China.
Jun JiangDepartment of Clinical Laboratory, Guangzhou Women and Children Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510600, P.R. China.
Chun-Yan YangDepartment of Clinical Laboratory, Guangzhou Women and Children Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510600, P.R. China.
Jin-Fu XuDepartment of Clinical Laboratory, Guangzhou Women and Children Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510600, P.R. China.
Qing HeDepartment of Clinical Laboratory, Guangzhou Women and Children Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510600, P.R. China.
Yan-Wei HuDepartment of Clinical Laboratory, Guangzhou Women and Children Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510600, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have reported the potential involvement of ferroptosis in the development of atherosclerosis (AS). Acyl-CoA synthetase long chain family member 4 (ACSL4) is an essential component in the promotion of ferroptosis. The present study aimed to investigate the role of ACSL4 and zinc finger translocation-associated protein (ZFTA) in the regulation of endothelial cell ferroptosis in AS. Human umbilical vein endothelial cells (HUVECs) with ACSL4 knockout were generated using CRISPR/Cas9 technology. To assess ferroptosis, malondialdehyde concentration, iron content and reactive oxygen species levels were quantified in the present study. In addition, western blot analysis was conducted to explore the potential mechanisms underlying ACSL4 and ZFTA in the modulation of ferroptosis in HUVECs. The results of the present study demonstrated that the expression levels of ACSL4 and ZFTA were significantly increased in human atherosclerotic plaques. In addition, ACSL4 knockout led to a reduced susceptibility to ferroptosis, while ZFTA contributed to ferroptosis in HUVECs. Results of the present study also demonstrated that ZFTA overexpression upregulated ACSL4 expression in HUVECs, whereas ZFTA knockdown led to decreased ACSL4 expression. Co-transfection experiments demonstrated that the ZTFA overexpression-mediated increase in ferroptosis was reversed following ACSL4 knockdown. Collectively, results of the present study highlighted that ACSL4 mediated the effects of ZFTA on the ferroptosis of HUVECs. Thus, the present study demonstrated the potential role of ACSL4 and ZFTA in the regulation of ferroptosis, and highlighted that ferroptosis-related pathways may act as potential targets in the treatment of AS.

Indexed as

acyl-CoA synthetase long chain family member 4atherosclerosisendothelial cellsferroptosiszinc finger translocation-associated protein

Identifiers

PMID39011065
PMCPMC11247542

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.