Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Homocysteine and vascular dysfunction

S R Lentz1

  • 1Veterans Affairs Medical Center, Iowa City, IA 52246, USA. steven-lentz@uiowa.edu

Life Sciences
|January 1, 1997
PubMed
Summary
This summary is machine-generated.

Elevated homocysteine (homocyst(e)ine) levels are linked to vascular disease risk. Research suggests homocysteine may directly harm blood vessels, potentially through oxidative stress, but more studies are needed.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Haemophilia clinical care and research needs: Assessing priorities.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Targeting platelet EPCR for better therapeutic factor VIIa activity.

Journal of thrombosis and haemostasis : JTH·2018
Same author

The small-molecule MERTK inhibitor UNC2025 decreases platelet activation and prevents thrombosis.

Journal of thrombosis and haemostasis : JTH·2017
Same author

Limit of detection and threshold for positivity of the Centers for Disease Control and Prevention assay for factor VIII inhibitors.

Journal of thrombosis and haemostasis : JTH·2017
Same author

Clinical and laboratory phenotype variability in type 2M von Willebrand disease.

Journal of thrombosis and haemostasis : JTH·2017
Same author

D-dimer levels and recurrence in patients with unprovoked VTE and a negative qualitative D-dimer test after treatment.

Thrombosis research·2016
Same journal

RPS20 phosphorylation acts as a molecular switch to integrate inflammatory and oxidative stress signals in sepsis.

Life sciences·2026
Same journal

Local lymphatic circulation disorder: A key promoter of tissue inflammation and organ fibrosis.

Life sciences·2026
Same journal

Gestational homocysteine exposure induces preeclampsia-like phenotypes and alters fetal neurodevelopmental gene expression via impaired decidualization.

Life sciences·2026
Same journal

SLFN11 binds DDX1 to counteract human mesenchymal stem/stromal cell senescence through inhibition of mTOR/eIF4E signaling pathway activation.

Life sciences·2026
Same journal

Corrigendum to "Adipose stem cells-derived microvesicles and chicken egg-derived exosomes attenuate cardiac ischemia/reperfusion injury through AKT/ERK/Nrf2/HO-1 axis to inhibit apoptosis and inflammation and restore autophagy" [Life Sci. 395 (2026) 124364].

Life sciences·2026
Same journal

MAGED1 stabilizes NEUROD1 to promote Per3 expression in the pineal gland.

Life sciences·2026
See all related articles

Area of Science:

  • Cardiovascular Science
  • Biochemistry
  • Vascular Biology

Background:

  • Elevated plasma homocysteine (homocyst(e)ine) is associated with increased risk of thrombotic and atherosclerotic vascular disease.
  • The causal role of homocyst(e)ine versus associated conditions in vascular disease remains unclear.
  • Dietary interventions to lower homocyst(e)ine are proposed for vascular disease prevention.

Purpose of the Study:

  • To investigate whether elevated plasma homocyst(e)ine concentration directly causes vascular disease.
  • To explore the mechanisms by which homocysteine may contribute to vascular dysfunction.
  • To evaluate the role of homocysteine-induced oxidant stress in endothelial dysfunction.

Main Methods:

  • Review of in vitro cell studies, animal models, and human studies on hyperhomocyst(e)inemia.

Related Experiment Videos

  • Analysis of findings related to endothelial phenotype alteration and reactive oxygen species generation.
  • Examination of evidence supporting homocysteine's role in atherosclerosis, thrombosis, and vasospasm.

    • Main Results:

    • In vitro studies suggest homocysteine may alter endothelial cell function, potentially via peroxide generation.
    • Animal and human models of hyperhomocyst(e)inemia show support for the hypothesis of homocysteine-induced endothelial dysfunction.
    • Endothelial dysfunction in hyperhomocyst(e)inemia may contribute to atherosclerosis and complications like thrombosis and vasospasm.

    Conclusions:

    • Homocysteine may directly contribute to vascular dysfunction and disease development.
    • Homocysteine-induced oxidant stress is a potential mechanism underlying endothelial dysfunction.
    • Future research should clarify the role of homocysteine versus associated conditions (e.g., folate deficiency) and the benefits of B vitamin supplementation.