Evidence map›Paper›PMID 30781581›Full record

ReviewInternational journal of molecular sciences2019

The Contribution of Homocysteine Metabolism Disruption to Endothelial Dysfunction: State-of-the-Art.

Ruben Esse, Madalena Barroso, Isabel Tavares de Almeida, Rita Castro

Open access · goldAbstract readReview
In one paragraph

Review 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 172 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
172citing papers in PubMed, 1 pooled it
28.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

172 citing papers in PubMed, 1 synthesis or guideline pooled it, 315 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  7. Review
  8. Review
  9. Risk of Retinal Vein Occlusion in Patients With Vitamin BJournal of vitreoretinal diseases · 2026
    Article
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  20. Accelerated epigenetic aging as a modifier of homocysteine-associated cognitive decline: Findings from NHANES.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article

112 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 3 countries.

Ruben EsseDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA. ruben.esse@gmail.com.
Madalena BarrosoUniversity Children's Research@Kinder-UKE, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. m.barroso@uke.de.ORCID 0000-0002-1600-890X
Isabel Tavares de AlmeidaLaboratory of Metabolism and Genetics, Faculty of Pharmacy, University of Lisbon, 1649-003 Lisbon, Portugal. italmeida@ff.ul.pt.
Rita CastroInstitute for Medicines and Pharmaceutical Sciences (iMed.UL), Faculty of Pharmacy, University of Lisbon, 1649-003 Lisbon, Portugal. mum689@psu.edu.ORCID 0000-0002-4585-0741
Boston University · USPennsylvania State University · USUniversität Hamburg · DEUniversity of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homocysteine (Hcy) is a sulfur-containing non-proteinogenic amino acid formed during the metabolism of the essential amino acid methionine. Hcy is considered a risk factor for atherosclerosis and cardiovascular disease (CVD), but the molecular basis of these associations remains elusive. The impairment of endothelial function, a key initial event in the setting of atherosclerosis and CVD, is recurrently observed in hyperhomocysteinemia (HHcy). Various observations may explain the vascular toxicity associated with HHcy. For instance, Hcy interferes with the production of nitric oxide (NO), a gaseous master regulator of endothelial homeostasis. Moreover, Hcy deregulates the signaling pathways associated with another essential endothelial gasotransmitter: hydrogen sulfide. Hcy also mediates the loss of critical endothelial antioxidant systems and increases the intracellular concentration of reactive oxygen species (ROS) yielding oxidative stress. ROS disturb lipoprotein metabolism, contributing to the growth of atherosclerotic vascular lesions. Moreover, excess Hcy maybe be indirectly incorporated into proteins, a process referred to as protein N-homocysteinylation, inducing vascular damage. Lastly, cellular hypomethylation caused by build-up of

Indexed as

AtherosclerosisCardiovascular DiseasesEndothelial CellsHomocysteineHumansHydrogen SulfideHyperhomocysteinemiaMethionineNitric OxideReactive Oxygen SpeciesS-AdenosylhomocysteineHomocysteineHydrogen SulfideMethionineNitric OxideReactive Oxygen SpeciesS-Adenosylhomocysteineatherosclerosiscellular methylationS-adenosylhomocysteine

Identifiers

PMID30781581
PMCPMC6412520
OpenAlexW2911271268

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.