ArticleKidney international2006
Is homocysteine an iron-dependent cardiovascular risk factor?
Article in Kidney international, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed, 16 citations in OpenAlex.
- Iron-dependent formation of homocysteine from methionine and other thioethers.European journal of clinical nutrition · 2007Trial
- Homocysteine-induced decrease in HUVEC cells' resistance to oxidative stress is mediated by Akt-dependent changes in iron metabolism.European journal of nutrition · 2021Article
- Impact of Iron and Homocysteine Levels on T Peak-to-End Interval and Tp-e/QT Ratio in Elite Athletes.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2016Article
- Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases.BMC medical genomics · 2009Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies of endothelial function suggest that adverse vascular effects of homocysteine are iron-dependent. Iron sucrose worsens and iron chelation eliminates homocysteine-associated decreases in flow-mediated dialation. There may be no vasculopathic effect of homocysteine without available reactive iron. Iron-dependent amplification of the vascular effects of homocysteine may be one of several mechanisms by which stored iron increases cardiac risk.
Indexed as
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What OpenQuestion holds
Registered trials
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.