ReviewOpen life sciences2023
Ferroptosis: A potential target of macrophages in plaque vulnerability.
Review in Open life sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 5 citations in OpenAlex.
- LLMs uncover 6M1@C60's therapeutic targets: inhibiting atherosclerotic progression via NRF2/HO-1/GPX4 axis-mediated ferroptosis suppression.Journal of nanobiotechnology · 2026Article
- Insights Into Macrophage Ferroptosis: Implications for Atherosclerosis.Cell proliferation · 2026Review
- Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026Review
- Homocysteine promotes ferroptosis through NCOA4-mediated ferritinophagy in THP-1 macrophages.Frontiers in physiology · 2026Article
- Decoding the crosstalk: interplay between macrophage programmed cell death networks and cholesterol efflux.Frontiers in cardiovascular medicine · 2026Review
- The Role of Ferroptosis and Cuproptosis in Tuberculosis Pathogenesis: Implications for Therapeutic Strategies.Current issues in molecular biology · 2025Review
- Identification and interaction analysis of hubgenes related to neutrophil ferroptosis in intracranial atherosclerotic stenosis.Genetics and molecular biology · 2025Article
- Recent advances in the interaction of ferroptosis and immune-mediated inflammation in cardiovascular disease: mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
- Ferroptosis-related exosomal non-coding RNAs: promising targets in pathogenesis and treatment of non-malignant diseases.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plaque vulnerability has been the subject of several recent studies aimed at reducing the risk of stroke and carotid artery stenosis. Atherosclerotic plaque development is a complex process involving inflammation mediated by macrophages. Plaques become more vulnerable when the equilibrium between macrophage recruitment and clearance is disturbed. Lipoperoxides, which are affected by iron levels in cells, are responsible for the cell death seen in ferroptosis. Ferroptosis results from lipoperoxide-induced mitochondrial membrane toxicity. Atherosclerosis in ApoE(-/-) mice is reduced when ferroptosis is inhibited and iron intake is limited. Single-cell sequencing revealed that a ferroptosis-related gene was substantially expressed in atherosclerosis-modeled macrophages. Since ferroptosis can be regulated, it offers hope as a non-invasive method of treating carotid plaque. In this study, we discuss the role of ferroptosis in atherosclerotic plaque vulnerability, including its mechanism, regulation, and potential future research directions.
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Identifiers
What OpenQuestion holds
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.