ArticleOpen medicine (Warsaw, Poland)2024
Lycopene inhibits pyroptosis of endothelial progenitor cells induced by ox-LDL through the AMPK/mTOR/NLRP3 pathway.
Article in Open medicine (Warsaw, Poland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Mechanistic Modulation of Autophagy by Bioactive Natural Products: Implications for Human Aging and Longevity.Nutrients · 2026Review
- Cross-regulation of autophagy and pyroptosis: a new perspective on the inflammatory microenvironment of atherosclerosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Eburicoic acid inhibits endothelial cell pyroptosis and retards the development of atherosclerosis through the Keap1/Nrf2/HO‑1/ROS pathway.Molecular medicine reports · 2025Article
- Erythrosine-induced hepatic biomarkers and histopathological changes in male rats: protective effects of lycopene and anthocyanin.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The malfunction of endothelial progenitor cells (EPCs) due to ox-LDL is a risk contributor for arteriosclerotic disease. Meanwhile, lycopene possesses anti-inflammatory and antioxidative qualities. This investigation aimed to determine if lycopene can protect EPCs from ox-LDL-induced damage and to elucidate the underlying mechanism. The effects of lycopene on the survival, migration, and tube-forming capacity of EPCs were determined via
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Registered trials
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