ArticleJournal of cellular and molecular medicine2025
Ecdysterone Alleviates Atherosclerosis by Inhibiting NCF2 and Inhibiting Ferroptosis Mediated by the PI3K/Akt/Nrf2 Pathway.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Cell-Type-Specific Regulation of Ferroptosis in Atherosclerosis: Mechanisms and Therapeutic Potential of Natural Products.Cell biochemistry and function · 2026Review
- Sesamin attenuates atherosclerosis by alleviating vascular endothelial ferroptosis-related injuryFrontiers in cell and developmental biology · 2026Article
- Research progress on targeted regulatory proteins in the prevention and treatment of atherosclerosis.Frontiers in immunology · 2026Review
- Integration of transcriptomics and machine learning to explore inflammatory characteristics and key oxidative stress-related molecules in nasal polyps.Frontiers in immunology · 2026Article
- A recombinant humanized type III collagen coating with anti-inflammatory and endothelialization-promoting effects for left atrial appendage closure devices.Regenerative biomaterials · 2026Article
- Inhibition of ferroptosis-related NCF2 blocks the progression of lupus nephritis by activating PPARα pathway.Hereditas · 2025Article
- Ferroptosis of Macrophages and Endothelial Cells in Atherosclerosis: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2025Review
- Molecular Insights into Oxidative-Stress-Mediated Cardiomyopathy and Potential Therapeutic Strategies.Biomolecules · 2025Review
- Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Ecdysterone (Ecd), an active ingredient in trianthema, has a strong anti-inflammatory effect. This study aimed to explore the potential mechanism by which Ecd improves atherosclerosis (AS). Here, we systematically investigated the mechanism of Ecd in human umbilical vein endothelial cells (HUVECs) treated with oxidised low-density lipoprotein (ox-LDL). In ox-LDL-treated HUVECs, Ecd promoted HUVEC viability as well as inhibited ferroptosis and the secretion of inflammatory factors (TNF-α, IL-6 and IL-1β). In addition, Ecd inhibited the expression of neutrophil cytoplasmic factor 2 (NCF2) and triggered the PI3K/AKT/Nrf2 signalling pathway, thereby alleviating the increase of ferroptosis in ox-LDL-treated HUVECs. More importantly, we constructed an AS mouse model by feeding ApoE
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Registered trials
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.