ReviewJournal of physiology and biochemistry2024
Role of ROS and autophagy in the pathological process of atherosclerosis.
Review in Journal of physiology and biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- The role of caveolin-1 in atherosclerosis and its molecular mechanism.Lipids in health and disease · 2026Review
- Ginkgolide C alleviates atherosclerosis via activating Nrf2 to inhibit ROS‑dependent NLRP3 inflammasome activation.International journal of molecular medicine · 2026Article
- Cell encapsulated biomaterials for translational medicine.Bioactive materials · 2026Review
- A bibliometric analysis of autophagy research in atherosclerosis over the past decade.Medicine · 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
- A double-duty champion: Eurycoma longifolia counters oxidative stress and unlocks autophagy to safeguard neurons and muscle cells.PloS one · 2026Article
- Homocysteine promotes ferroptosis through NCOA4-mediated ferritinophagy in THP-1 macrophages.Frontiers in physiology · 2026Article
- Inhibitory Effect of Sirtuin6 on EndMT by Regulating Oxidative Stress and Autophagy in Coxsackievirus B3-Induced Cardiac Endothelial Cells.Immunity, inflammation and disease · 2025Article
- Nano-therapeutics targeting the macrophage-based microenvironment in the treatment of atherosclerosis.Journal of translational medicine · 2025Review
- Biological Modulation of Autophagy by Nanoplastics: A Current Overview.International journal of molecular sciences · 2025Review
- Review
- Macrophage pyroptosis in atherosclerosis: therapeutic potential.Acta biochimica et biophysica Sinica · 2025Review
- The potential mechanism of celastrol attenuating atherosclerosis by promoting macrophage autophagy via AMPK/ULK1 pathway.Frontiers in pharmacology · 2025Article
- FBXO38 Regulates Nox1 Stability to Reduce Vascular Endothelial Damage Induced by Low Oscillatory Shear Stress.Cardiovascular therapeutics · 2025Article
- Exercise in atherosclerosis: its beneficial effects and underlying mechanism.Frontiers in cell and developmental biology · 2025Review
- Abnormal lipid metabolism and atherosclerosis: a new perspective on organelle function regulation and ferroptosis.Frontiers in immunology · 2025Article
- Vulnerable plaques in atherosclerosis: focus on angiogenesis-associated phenotypic crosstalk.Frontiers in pharmacology · 2025Review
- The Effects of the oxLDL/β2GPI/anti-β2GPI Complex on Macrophage Autophagy and its Mechanism.Immunity, inflammation and disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Activation of autophagy and production of reactive oxygen species occur at various stages of atherosclerosis. To clarify the role and mechanism of autophagy and reactive oxygen species in atherosclerosis is of great significance to the prevention and treatment of atherosclerosis. Recent studies have shown that basal autophagy plays an important role in protecting cells from oxidative stress, reducing apoptosis and enhancing atherosclerotic plaque stability. Autophagy deficiency and excessive accumulation of reactive oxygen species can impair the function of endothelial cells, macrophages and smooth muscle cells, trigger autophagic cell death, and lead to instability and even rupture of plaques. However, the main signaling pathways regulating autophagy, the molecular mechanisms of autophagy and reactive oxygen species interaction, how they are initiated and distributed in plaques, and how they affect atherosclerosis progression, remain to be clarified. At present, there is no autophagy inducer used to treat atherosclerosis clinically. Therefore, it is urgent to clarify the mechanism of autophagy and find new targets for autophagy. Antioxidant agents generally have defects such as low reactive oxygen species scavenging efficiency and high cytotoxicity. Highly potent autophagy inducers and reactive oxygen species scavengers still need to be further developed and validated to provide more possibilities for innovative treatments for atherosclerosis.
Indexed as
Identifiers
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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.