ArticleArteriosclerosis, thrombosis, and vascular biology2005
Hyperhomocystinemia impairs endothelial function and eNOS activity via PKC activation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 141 citations in OpenAlex.
- Independent and Joint Associations of Lipoprotein(a) and Homocysteine with Carotid-Femoral Pulse-Wave Velocity in Adults with Treated Hypertension: A Single-Centre Cross-Sectional Study.Journal of clinical medicine · 2026Article
- Role of hyperhomocysteinemia in atherosclerosis: from bench to bedside.Annals of medicine · 2025Review
- Higher homocysteine and fibrinogen are associated with early-onset post-stroke depression in patients with acute ischemic stroke.Frontiers in psychiatry · 2024Article
- Early hyperlipidemia triggers metabolomic reprogramming with increased SAH, increased acetyl-CoA-cholesterol synthesis, and decreased glycolysis.Redox biology · 2023Article
- Glycyrrhizic Acid Inhibits High-Mobility Group Box-1 and Homocysteine-Induced Vascular Dysfunction.Nutrients · 2023Article
- Epigenetic Regulation by microRNAs in Hyperhomocysteinemia-Accelerated Atherosclerosis.International journal of molecular sciences · 2022Review
- Homocysteine predicts vascular target organ damage in hypertension and may serve as guidance for first-line antihypertensive therapy.Journal of clinical hypertension (Greenwich, Conn.) · 2021Article
- Homocysteine and Age-Related Central Nervous System Diseases: Role of Inflammation.International journal of molecular sciences · 2021Review
- The Effects of Medicinal Plants and Bioactive Natural Compounds on Homocysteine.Molecules (Basel, Switzerland) · 2021Review
- Aortic Dimensions, Biophysical Properties, and Plasma Biomarkers in Children and Adults with Marfan or Loeys-Dietz Syndrome.CJC open · 2021Article
- Homocysteine alters vasoreactivity of human internal mammary artery by affecting the KAnnals of translational medicine · 2021Article
- Homocysteine Causes Endothelial Dysfunction via Inflammatory Factor-Mediated Activation of Epithelial Sodium Channel (ENaC).Frontiers in cell and developmental biology · 2021Article
- Novel Knowledge-Based Transcriptomic Profiling of Lipid Lysophosphatidylinositol-Induced Endothelial Cell Activation.Frontiers in cardiovascular medicine · 2021Article
- Exploring the role of dimethylarginine dimethylaminohydrolase-mediated reduction in tissue asymmetrical dimethylarginine levels in cardio-protective mechanism of ischaemic postconditioning in rats.Iranian journal of basic medical sciences · 2019Article
- Hydrogen Sulfide Protects Hyperhomocysteinemia-Induced Renal Damage by Modulation of Caveolin and eNOS Interaction.Scientific reports · 2019Article
- Hydrogen Sulfide: A Therapeutic Option in Systemic Sclerosis.International journal of molecular sciences · 2018Review
- Pioglitazone restores the homocysteine‑impaired function of endothelial progenitor cells via the inhibition of the protein kinase C/NADPH oxidase pathway.Molecular medicine reports · 2018Article
- A20 alleviates the vascular remodeling induced by homocysteine.American journal of translational research · 2018Article
- Hyperhomocysteinemia as a Risk Factor for Vascular Contributions to Cognitive Impairment and Dementia.Frontiers in aging neuroscience · 2018Review
- Hesperidin, a citrus flavonoid, protects against l-methionine-induced hyperhomocysteinemia by abrogation of oxidative stress, endothelial dysfunction and neurotoxicity in Wistar rats.Pharmaceutical biology · 2017Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
objectiveA risk factor for cardiovascular disease, hyperhomocystinemia (HHcy), is associated with endothelial dysfunction. In this study, we examined the mechanistic role of HHcy in endothelial dysfunction. METHODS AND
resultsThrough the use of 2 functional models, aortic rings and intravital video microscopy of the cremaster, we found that arterial relaxation in response to the endothelium-dependent vessel relaxant, acetylcholine or the nitric oxide synthase (NOS) activator (A23187), was significantly impaired in cystathionine beta-synthase null (CBS(-/-)) mice. However, the vascular smooth muscle cell (VSMC) response to the nitric oxide (NO) donor (SNAP) was preserved in CBS(-/-) mice. In addition, superoxide dismutase and catalase failed to restore endothelium-dependent vasodilatation. Endothelial nitric oxide synthase (eNOS) activity was significantly reduced in mouse aortic endothelial cells (MAECs) of CBS(-/-) mice, as well as in Hcy-treated mouse and human aortic endothelial cells (HAECs). Hcy-mediated eNOS inhibition--which was not rescued by adenoviral transduction of superoxide dismutase and glutathione peroxidase, or by tetrahydrobiopterin, sepiapterin, and arginine supplementations in MAEC--was associated with decreased protein expression and increased threonine 495 phosphorylation of eNOS in HAECs. Ultimately, a protein kinase C (PKC) inhibitor, GF109203X (GFX), reversed Hcy-mediated eNOS inactivation and threonine 495 phosphorylation in HAECs.
conclusionsThese data suggest that HHcy impairs endothelial function and eNOS activity, primarily through PKC activation.
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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.