ArticleInternational journal of molecular sciences2019
KRIT1 Deficiency Promotes Aortic Endothelial Dysfunction.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Unveiling a Novel Molecular Interaction and Pro-Metastatic Signaling Cascades Driven by KRIT1.International journal of molecular sciences · 2026Article
- The Role of Immune Infiltration and Oxidative Stress in the Progression of Cerebral Cavernous Malformation.Brain and behavior · 2026Review
- Lectin-type oxidized LDL receptor-1 as a potential therapeutic target for cerebral cavernous malformations treatment.Frontiers in neuroscience · 2024Article
- KRIT1: A Traffic Warden at the Busy Crossroads Between Redox Signaling and the Pathogenesis of Cerebral Cavernous Malformation Disease.Antioxidants & redox signaling · 2023Review
- Multidrug-Loaded Lipid Nanoemulsions for the Combinatorial Treatment of Cerebral Cavernous Malformation Disease.Biomedicines · 2023Article
- Distant Recurrence of a Cerebral Cavernous Malformation in the Vicinity of a Developmental Venous Anomaly: Case Report of Local Oxy-Inflammatory Events.International journal of molecular sciences · 2022Article
- Heterozygous Loss of KRIT1 in Mice Affects Metabolic Functions of the Liver, Promoting Hepatic Oxidative and Glycative Stress.International journal of molecular sciences · 2022Article
- Agri-Food Waste from Apple, Pear, and Sugar Beet as a Source of Protective Bioactive Molecules for Endothelial Dysfunction and Its Major Complications.Antioxidants (Basel, Switzerland) · 2022Review
- mPR-Specific Actions Influence Maintenance of the Blood-Brain Barrier (BBB).International journal of molecular sciences · 2022Article
- Next-Generation Sequencing Advances the Genetic Diagnosis of Cerebral Cavernous Malformation (CCM).Antioxidants (Basel, Switzerland) · 2022Article
- Well-Known and Novel Players in Endothelial Dysfunction: Updates on a Notch(ed) Landscape.Biomedicines · 2021Review
- Protein kinase Cα regulates the nucleocytoplasmic shuttling of KRIT1.Journal of cell science · 2021Article
- COX-2 Is Downregulated in Human Stenotic Aortic Valves and Its Inhibition Promotes Dystrophic Calcification.International journal of molecular sciences · 2020Article
- A Review of the Relationship Between CTRP Family and Coronary Artery Disease.Current atherosclerosis reports · 2020Review
- Vitamin D Deficiency and the Risk of Cerebrovascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Transplacental arsenic exposure produced 5-methylcytosine methylation changes and aberrant microRNA expressions in livers of male fetal mice.Toxicology · 2020Article
- Dicarbonyl Stress and S-Glutathionylation in Cerebrovascular Diseases: A Focus on Cerebral Cavernous Malformations.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Loss-of-function mutations of the gene encoding Krev interaction trapped protein 1 (KRIT1) are associated with the pathogenesis of Cerebral Cavernous Malformation (CCM), a major cerebrovascular disease characterized by abnormally enlarged and leaky capillaries and affecting 0.5% of the human population. However, growing evidence demonstrates that KRIT1 is implicated in the modulation of major redox-sensitive signaling pathways and mechanisms involved in adaptive responses to oxidative stress and inflammation, suggesting that its loss-of-function mutations may have pathological effects not limited to CCM disease. The aim of this study was to address whether KRIT1 loss-of-function predisposes to the development of pathological conditions associated with enhanced endothelial cell susceptibility to oxidative stress and inflammation, such as arterial endothelial dysfunction (ED) and atherosclerosis. Silencing of KRIT1 in human aortic endothelial cells (HAECs), coronary artery endothelial cells (HCAECs), and umbilical vein endothelial cells (HUVECs) resulted in increased expression of endothelial proinflammatory adhesion molecules vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) and in enhanced susceptibility to tumor necrosis factor alpha (TNF-α)-induced apoptosis. These effects were associated with a downregulation of Notch1 activation that could be rescued by antioxidant treatment, suggesting that they are consequent to altered intracellular redox homeostasis induced by KRIT1 loss-of-function. Furthermore, analysis of the aorta of heterozygous
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Registered trials
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