ArticlePloS one2014
Caveolin-1 is a critical determinant of autophagy, metabolic switching, and oxidative stress in vascular endothelium.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 127 citations in OpenAlex.
- Article
- Caveolin-1: an ambiguous entity in breast cancer.Molecular cancer · 2025Review
- Lysyl-tRNA synthetase 1 promotes atherogenesis via autophagy-related secretion and inflammation.Scientific reports · 2025Article
- Targeting secretory autophagy in solid cancers: mechanisms, immune regulation and clinical insights.Experimental hematology & oncology · 2025Review
- The crosstalk of caveolin-1 and autophagy in different diseases.Frontiers in immunology · 2025Review
- Low caveolin-1 levels and symptomatic intracranial haemorrhage risk in large-vessel occlusive stroke patients after endovascular thrombectomy.European journal of neurology · 2024Article
- Article
- Cell death in atherosclerosis.Cell cycle (Georgetown, Tex.) · 2024Review
- Article
- Role of caveolin-1 in metabolic programming of fetal brain.iScience · 2023Article
- Proteostasis and resilience in the mechanically-stressed vascular endothelium.Current opinion in physiology · 2023Review
- Review
- Metabolic Deregulation in Pulmonary Hypertension.Current issues in molecular biology · 2023Article
- The prognostic value of caveolin-1 levels in ischemic stroke patients after mechanical thrombectomy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Lemon-Derived Extracellular Vesicles Nanodrugs Enable to Efficiently Overcome Cancer Multidrug Resistance by Endocytosis-Triggered Energy Dissipation and Energy Production Reduction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Review
- 3β-Hydroxy-5β-hydroxy-B-norcholestane-6β-carboxaldehyde (SEC-B) Induces Proinflammatory Activation of Human Endothelial Cells Associated with Nitric Oxide Production and Endothelial Nitric Oxide Synthase/Caveolin-1 Dysregulation.Antioxidants (Basel, Switzerland) · 2022Article
- Caveolin-1 controls mitochondrial damage and ROS production by regulating fission - fusion dynamics and mitophagy.Redox biology · 2022Article
- Endothelial Cell Metabolism in Vascular Functions.Cancers · 2022Review
- Caveolin-1 Regulation and Function in Mouse Uterus during Early Pregnancy and under Human In Vitro Decidualization.International journal of molecular sciences · 2022Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Caveolin-1 is a scaffolding/regulatory protein that interacts with diverse signaling molecules. Caveolin-1(null) mice have marked metabolic abnormalities, yet the underlying molecular mechanisms are incompletely understood. We found the redox stress plasma biomarker plasma 8-isoprostane was elevated in caveolin-1(null) mice, and discovered that siRNA-mediated caveolin-1 knockdown in endothelial cells promoted significant increases in intracellular H₂O₂. Mitochondrial ROS production was increased in endothelial cells after caveolin-1 knockdown; 2-deoxy-D-glucose attenuated this increase, implicating caveolin-1 in control of glycolytic pathways. We performed unbiased metabolomic characterizations of endothelial cell lysates following caveolin-1 knockdown, and discovered strikingly increased levels (up to 30-fold) of cellular dipeptides, consistent with autophagy activation. Metabolomic analyses revealed that caveolin-1 knockdown led to a decrease in glycolytic intermediates, accompanied by an increase in fatty acids, suggesting a metabolic switch. Taken together, these results establish that caveolin-1 plays a central role in regulation of oxidative stress, metabolic switching, and autophagy in the endothelium, and may represent a critical target in cardiovascular diseases.
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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.