ReviewCurrent atherosclerosis reports2006
Nonconventional genetic risk factors for cardiovascular disease.
Review in Current atherosclerosis reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Functional analysis of 5-lipoxygenase promoter repeat variants.Human molecular genetics · 2009Trial
- Chronic apical periodontitis exacerbates atherosclerosis in apolipoprotein E-deficient mice and leads to changes in the diversity of gut microbiota.International endodontic journal · 2022Article
- Evaluation of the role of opium addiction in acute myocardial infarction as a risk factor.Caspian journal of internal medicine · 2013Article
- Association of PLA2G4A with myocardial infarction is modulated by dietary PUFAs.The American journal of clinical nutrition · 2012Article
- Genetic contribution of the leukotriene pathway to coronary artery disease.Human genetics · 2011Article
- Polyunsaturated fatty acids and cardiovascular disease: implications for nutrigenetics.Journal of nutrigenetics and nutrigenomics · 2009Review
- Nutrigenetic association of the 5-lipoxygenase gene with myocardial infarction.The American journal of clinical nutrition · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Despite numerous advances made in identifying the genes for rare mendelian forms of cardiovascular disease (CVD), relatively little is known about the common, complex forms at the genetic level. Moreover, most genes that have been associated with CVD, whether they are single gene forms or more common forms of the disease, have primarily been involved in biochemical pathways related to what are considered "conventional" risk factors. However, recent genetic studies have begun to identify genes and pathways associated with CVD that would not be considered to underlie conventional risk factors. In this review, we discuss the evidence for this latter notion based on recent linkage and association studies in humans. As an example, we also illustrate how a combination of mouse and human genetics led to identification of the 5-lipoxygenase pathway for CVD, with potentially important implications for its treatment and diagnosis. We conclude with a discussion of the prospects for identifying CVD genes in the future and for potentially developing more effective therapeutic strategies.
Indexed as
Identifiers
16640955What 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.