ArticleJournal of lipid research2019
Lysosomal oxidation of LDL alters lysosomal pH, induces senescence, and increases secretion of pro-inflammatory cytokines in human macrophages.
Article in Journal of lipid research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Review of OxLDL Driven Inflammatory Cell Activation.Current atherosclerosis reports · 2025Pooled it
- Hypertriglyceridaemia and its multifaceted mechanisms driving atherosclerotic cardiovascular disease.Lipids in health and disease · 2026Review
- Quantum sensing of free radicals in macrophages reveals early autophagy-lysosome regulation in an atherosclerosis cell model.Redox biology · 2025Article
- Senescent macrophages in tumor: phenotypes, roles, and interventions.Cell death & disease · 2025Review
- Lysosomes in the immunometabolic reprogramming of immune cells in atherosclerosis.Nature reviews. Cardiology · 2025Review
- Machine learning-driven insights into lipid metabolism and inflammatory pathways in knee osteoarthritis.Frontiers in nutrition · 2025Article
- Cross-Disease Identification of FBP1 in Atherosclerosis and Calcific Aortic Valve Disease via Integrated Bioinformatics and Validation: Functional Analysis and Therapeutic Target Exploration.Journal of inflammation research · 2025Article
- Obesity modulates NK cell activity via LDL and DUSP1 signaling for populations with adverse social determinants.JCI insight · 2024Article
- Decoding marker genes and immune landscape of unstable carotid plaques from cellular senescence.Scientific reports · 2024Article
- Review
- Dysregulated lipid metabolism and intervertebral disc degeneration: the important role of ox-LDL/LOX-1 in endplate chondrocyte senescence and calcification.Molecular medicine (Cambridge, Mass.) · 2024Article
- Macrophage senescence in health and diseases.Acta pharmaceutica Sinica. B · 2024Review
- Association ofPeerJ · 2024Article
- Enhancement of Radiation Sensitivity by Cathepsin L Suppression in Colon Carcinoma Cells.International journal of molecular sciences · 2023Article
- The Significance of Cathepsin B in Mediating Radiation Resistance in Colon Carcinoma Cell Line (Caco-2).International journal of molecular sciences · 2023Article
- Pathological alterations in the expression status of rotator cuff tendon matrix components in hyperlipidemia.Molecular and cellular biochemistry · 2023Article
- Therapeutic opportunities for senolysis in cardiovascular disease.The FEBS journal · 2023Review
- Hypoxia promotes EV secretion by impairing lysosomal homeostasis in HNSCC through negative regulation of ATP6V1A by HIF-1α.Journal of extracellular vesicles · 2023Article
- Impact of Enniatin B and Beauvericin on Lysosomal Cathepsin B Secretion and Apoptosis Induction.International journal of molecular sciences · 2023Article
- Efficacy and underlying mechanisms of berberine against lipid metabolic diseases: a review.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have shown that aggregated LDL is internalized by macrophages and oxidized in lysosomes by redox-active iron. We have now investigated to determine whether the lysosomal oxidation of LDL impairs lysosomal function and whether a lysosomotropic antioxidant can prevent these alterations. LDL aggregated by SMase (SMase-LDL) caused increased lysosomal lipid peroxidation in human monocyte-derived macrophages or THP-1 macrophage-like cells, as shown by a fluorescent probe, Foam-LPO. The pH of the lysosomes was increased considerably by lysosomal LDL oxidation as shown by LysoSensor Yellow/Blue and LysoTracker Red. SMase-LDL induced senescence-like properties in the cells as shown by β-galactosidase staining and levels of p53 and p21. Inflammation plays a key role in atherosclerosis. SMase-LDL treatment increased the lipopolysaccharide-induced secretion of TNF-α, IL-6, and MCP-1. The lysosomotropic antioxidant, cysteamine, inhibited all of the above changes. Targeting lysosomes with antioxidants, such as cysteamine, to prevent the intralysosomal oxidation of LDL might be a novel therapy for atherosclerosis.
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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 Socratic graph.