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

ADMA and hyperhomocysteinemia.

Sanjana Dayal1, Steven R Lentz

  • 1Department of Internal Medicine, University of Iowa, Iowa City 52242, USA.

Vascular Medicine (London, England)
|February 1, 2006
PubMed
Summary
This summary is machine-generated.

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

Age and sex dependent shift in murine gut microbiome reveals pathological links to host cardiovascular and metabolic pathways.

GeroScience·2026
Same author

Mim8 Bispecific Antibody Prophylaxis in Hemophilia A with or without Inhibitors.

The New England journal of medicine·2026
Same author

Cardiovascular, renal and pulmonary risks of Long COVID: a retrospective cohort study stratified by age and sex.

medRxiv : the preprint server for health sciences·2026
Same author

Mitochondrial oxidants promote platelet activation and thrombotic susceptibility in prediabetes.

The Journal of clinical investigation·2025
Same author

Platelet defects in patients and mice with Ehlers-Danlos syndrome.

Blood·2025
Same author

FRONTIER1 multiple ascending dose extension: a safety, tolerability, pharmacokinetics, and pharmacodynamics study of Mim8 in people with hemophilia A.

Research and practice in thrombosis and haemostasis·2025
Same journal

Images in Vascular Medicine: When coronary anatomy goes the wrong way-A diagnostic challenge.

Vascular medicine (London, England)·2026
Same journal

Home-based intravenous iloprost by portable elastomeric pump in chronic limb-threatening ischemia: A pilot study.

Vascular medicine (London, England)·2026
Same journal

Vascular Disease Patient Information Page: Renal denervation.

Vascular medicine (London, England)·2026
Same journal

Relations of Life's Essential 8 score with arterial and microvascular function: The Jackson Heart Study.

Vascular medicine (London, England)·2026
Same journal

Generalizability of the CREST‑2 trial: A real‑world analysis.

Vascular medicine (London, England)·2026
Same journal

Downhill-walking exercise training in a patient with symptomatic peripheral artery disease: A case report.

Vascular medicine (London, England)·2026
See all related articles

High homocysteine levels (hyperhomocysteinemia) contribute to cardiovascular disease by impairing nitric oxide (NO) availability. Asymmetric dimethylarginine (ADMA) elevation appears to be a key mechanism linking hyperhomocysteinemia to endothelial dysfunction.

Area of Science:

  • Cardiovascular Science
  • Endothelial Biology
  • Metabolic Disorders

Background:

  • Hyperhomocysteinemia is a known risk factor for cardiovascular disease and stroke.
  • Endothelial dysfunction, characterized by impaired nitric oxide (NO) bioavailability, is a common feature of cardiovascular risk factors.
  • The precise molecular mechanisms underlying NO reduction in hyperhomocysteinemia are not fully elucidated.

Purpose of the Study:

  • To investigate the role of asymmetric dimethylarginine (ADMA) as a potential mediator of endothelial dysfunction in hyperhomocysteinemia.
  • To explore the relationship between homocysteine, ADMA metabolism, and NO bioavailability.
  • To provide mechanistic insights into the impact of ADMA on hyperhomocysteinemia-induced vascular impairment.

Main Methods:

Related Experiment Videos

  • Review of existing animal and clinical studies examining plasma total homocysteine, plasma ADMA, and endothelial function.
  • Analysis of the biochemical pathways involving homocysteine, ADMA synthesis, and dimethylarginine dimethylaminohydrolase (DDAH) activity.
  • Consideration of data from transgenic mouse models with modified ADMA metabolism.

    • Main Results:

    • Strong associations observed between elevated plasma total homocysteine, plasma ADMA levels, and the presence of endothelial dysfunction.
    • Evidence suggests homocysteine can interfere with ADMA metabolism by inhibiting DDAH.
    • A model is proposed where increased ADMA levels serve as a unifying factor for endothelial dysfunction in hyperhomocysteinemia.

    Conclusions:

    • Elevated ADMA may be a critical mediator of endothelial dysfunction associated with hyperhomocysteinemia.
    • Understanding ADMA's role offers potential therapeutic targets for cardiovascular disease prevention.
    • Further research using advanced models is expected to clarify the intricate mechanisms involved.