ArticleCirculation research2026
Functional Genomics Link REST to Endothelial Plasticity and Atherosclerosis.
Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- ERG preserves endothelial identity to limit atherosclerosis.Nature communications · 2026Article
- RE1-Silencing Transcription Factor: an Atheroprotective Regulator in the Vascular Endothelium.Journal of cardiovascular translational research · 2026Article
- Sex differences in nerve injury-induced neuropathic pain via REST in primary sensory neurons.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
backgroundGenome-wide association studies have identified multiple novel loci that contribute to coronary artery disease pathogenesis, but the mechanisms of these associations remain largely unknown.
methodsIn this study, we used a multitrait colocalization approach to prioritize novel endothelial-specific loci for atherosclerosis. We combined computational methods with in vitro assays and mouse models to study one of those new loci targeting the gene REST (RE1-silencing transcription factor).
resultsA multitrait colocalization approach across expression quantitative trait loci in atherosclerosis-relevant cell types, followed by in vitro CRISPR interference, revealed that a conserved regulatory element in a chromosome 4 genetic locus increases the risk of coronary artery disease and decreases the expression of REST, a transcriptional repressor, in endothelial cells.
conclusionsIn summary, our data reveal the novel role of REST as a repressor in endothelial cells that functions to constitutively inhibit endothelial-to-mesenchymal transition and protect against atherosclerosis.
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.