ReviewProteomics. Clinical applications2014
Epigenomes: the missing heritability in human cardiovascular disease?
Review in Proteomics. Clinical applications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled 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.
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
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- A systematic literature review on the European, African and Amerindian genetic ancestry components on Brazilian health outcomes.Scientific reports · 2019Pooled it
- Unravelling the genetic architecture of cardiovascular disease through structural variant detection with whole-genome sequencing.Frontiers in genetics · 2026Review
- Screening of immune-related biological markers for aneurysmal subarachnoid hemorrhage based on machine learning approaches.Biochemistry and biophysics reports · 2023Article
- Cross-sectional metabolic subgroups and 10-year follow-up of cardiometabolic multimorbidity in the UK Biobank.Scientific reports · 2022Article
- Associations of ARHGAP26 Polymorphisms with Alzheimer's Disease and Cardiovascular Disease.Journal of molecular neuroscience : MN · 2022Article
- Article
- Maternal Pre-Pregnancy Cardiovascular Risk Factors and Offspring and Grandoffspring Health: Bogalusa Daughters.International journal of environmental research and public health · 2018Article
- Relationship of disease-associated gene expression to cardiac phenotype is buffered by genetic diversity and chromatin regulation.Physiological genomics · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiovascular disease is a tremendous burden on human health and results from malfunction of various networks of biological molecules in the context of environmental stress. Despite strong evidence of heritability, many common forms of heart disease (heart failure in particular) have not yielded to genome-wide association studies to identify causative mutations acting via the disruption of individual molecules. Increasing evidence suggests, however, that genetic variation in noncoding regions is strongly linked to disease susceptibility. We hypothesize that epigenomic variation may engender different chromatin environments in the absence of (or in parallel with) changes in protein or mRNA sequence and abundance. In this manner, distinct-genetically encoded-chromatin environments can exhibit distinct responses to environmental stresses that cause heart failure, explaining a significant portion of the altered susceptibility that is observed in human disease.
Indexed as
Identifiers
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.