ArticleCytotechnology2024
KLF7 reverses ox-LDL-induced ferroptosis in HMEC-1 cells through transcriptionally activating ALKBH5 to inhibit the m6A modification of ACSL4.
Article in Cytotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- MicroRNA-425-5p as a diagnostic biomarker and ox-LDL-induced VSMC regulator in atherosclerosis.Journal of cardiothoracic surgery · 2026Article
- Decoding the Kruppel-like Transcription Factors in Atherosclerosis: Insight from Molecular and Translational Perspectives.International journal of molecular sciences · 2025Review
- Pharmacological and toxicological roles of Kruppel-like factors (KLFs) in the cardiovascular system: a review.Molecular biology reports · 2025Review
- Emerging mechanisms and implications of m6A in CVDs: potential applications of natural products.Frontiers in cardiovascular medicine · 2025Review
- Bushen Huoxue prescription inhibits ferroptosis of HUVEC cells by regulating FABP1-mediated lipid metabolism.Frontiers in pharmacology · 2025Article
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Authors and funding
4 authors.
Funding
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Abstract
Atherosclerosis is a chronic inflammatory vascular disease. It was confirmed that activation of ferroptosis could induce the development of AS. Meanwhile, Krüppel-like factor 7 was reported to be involved in AS. Nevertheless, the detailed function of KLF7 in ferroptosis during AS has not been not explored. To mimic AS in vitro, human microvascular endothelial cells (HMEC-1) were exposed to 100 μg/mL ox-LDL. Cell viability was tested using MTT assay, and commercial kits were applied to examine the ferroptosis. Flow cytometry was applied for testing lipid ROS level. The relation between KLF7 and AlkB homolog 5 (ALKBH5) was explored using dual luciferase and ChIP assays. Furthermore, MeRIP was used to test the m6A modification level of ACSL4. KLF7 and ALKBH5 overexpression reversed ox-LDL-induced ferroptosis (characterized by up-regulated MDA, iron, Fe
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