ArticlePLoS genetics2015
Coronary Artery Disease Associated Transcription Factor TCF21 Regulates Smooth Muscle Precursor Cells That Contribute to the Fibrous Cap.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 101 citations in OpenAlex.
- Article
- Review
- Single-cell RNA-sequencing reveals adventitial fibroblast alterations during mouse atherosclerosis.Atherosclerosis · 2025Article
- Tcf21 modulates fibroblast activation and promotes cardiac fibrosis after injury via Pdgfrb signaling.Scientific reports · 2025Article
- Integrative in Silico and in vitro validation suggest LINC00963 and SNHG15 as candidate biomarkers for coronary artery disease.Scientific reports · 2025Article
- Transcription Factor 21 Regulates Cardiac Myofibroblast Formation and Fibrosis.Circulation research · 2025Article
- Review
- Deep learning-derived splenic radiomics, genomics, and coronary artery disease.medRxiv : the preprint server for health sciences · 2024Article
- Translatome profiling reveals Itih4 as a novel smooth muscle cell-specific gene in atherosclerosis.Cardiovascular research · 2024Article
- Review
- Transcription factor Tcf21 modulates urinary bladder size and differentiation.Development, growth & differentiation · 2024Article
- Modulation of Smooth Muscle Cell Phenotype for Translation of Tissue-Engineered Vascular Grafts.Tissue engineering. Part B, Reviews · 2023Review
- Molecular mechanisms of coronary artery disease risk at the PDGFD locus.Nature communications · 2023Article
- Molecular mechanisms of coronary artery disease risk at thebioRxiv : the preprint server for biology · 2023Article
- TXNIP Suppresses the Osteochondrogenic Switch of Vascular Smooth Muscle Cells in Atherosclerosis.Circulation research · 2023Article
- Transcription factors: key regulatory targets of vascular smooth muscle cell in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2023Review
- Mechanisms of fibrous cap formation in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- Article
- Dynamic changes in chromatin accessibility are associated with the atherogenic transitioning of vascular smooth muscle cells.Cardiovascular research · 2022Article
- Effects of Coronary Artery Disease-Associated Variants on Vascular Smooth Muscle Cells.Circulation · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 4 institutions in 2 countries.
Funding
Abstract
Recent genome wide association studies have identified a number of genes that contribute to the risk for coronary heart disease. One such gene, TCF21, encodes a basic-helix-loop-helix transcription factor believed to serve a critical role in the development of epicardial progenitor cells that give rise to coronary artery smooth muscle cells (SMC) and cardiac fibroblasts. Using reporter gene and immunolocalization studies with mouse and human tissues we have found that vascular TCF21 expression in the adult is restricted primarily to adventitial cells associated with coronary arteries and also medial SMC in the proximal aorta of mouse. Genome wide RNA-Seq studies in human coronary artery SMC (HCASMC) with siRNA knockdown found a number of putative TCF21 downstream pathways identified by enrichment of terms related to CAD, including "vascular disease," "disorder of artery," and "occlusion of artery," as well as disease-related cellular functions including "cellular movement" and "cellular growth and proliferation." In vitro studies in HCASMC demonstrated that TCF21 expression promotes proliferation and migration and inhibits SMC lineage marker expression. Detailed in situ expression studies with reporter gene and lineage tracing revealed that vascular wall cells expressing Tcf21 before disease initiation migrate into vascular lesions of ApoE-/- and Ldlr-/- mice. While Tcf21 lineage traced cells are distributed throughout the early lesions, in mature lesions they contribute to the formation of a subcapsular layer of cells, and others become associated with the fibrous cap. The lineage traced fibrous cap cells activate expression of SMC markers and growth factor receptor genes. Taken together, these data suggest that TCF21 may have a role regulating the differentiation state of SMC precursor cells that migrate into vascular lesions and contribute to the fibrous cap and more broadly, in view of the association of this gene with human CAD, provide evidence that these processes may be a mechanism for CAD risk attributable to the vascular wall.
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.