ArticleNature cardiovascular research2025
PRDM16 regulates smooth muscle cell identity and atherosclerotic plaque composition.
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed.
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Steroid hormone antagonism affords vascular protection in a mouse model of vascular Ehlers-Danlos syndrome.JCI insight · 2026Article
- Epigenetic regulation in atherosclerosis and its therapeutic potential.Nature reviews. Cardiology · 2026Review
- Multimodal atlas of human atherosclerosis links granular vascular cell states to coronary artery disease risk.medRxiv : the preprint server for health sciences · 2026Article
- Coronary artery disease risk gene PRDM16 regulates smooth muscle homeostasis.Journal of molecular and cellular cardiology · 2026Article
- Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target.Cells · 2026Review
- The cardiovascular-immune axis: crosstalk and therapy in atherosclerosis, myocarditis and vasculitis.Frontiers in immunology · 2026Review
- Single cell spatial transcriptomics integration deciphers the morphological heterogeneity of atherosclerotic carotid arteries.Nature communications · 2025Article
- Flipping the PRDM16 switch in 'multifunctional mesenchymes' may help to define atherosclerotic plaque.Nature cardiovascular research · 2025Article
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Abstract
Vascular smooth muscle cells (SMCs) undergo phenotype switching to acquire various fates in response to pathological stimuli. Among these, 'synthetic' SMCs-defined by migration, proliferation and extracellular matrix production-accumulate in atherosclerotic lesions and contribute to fibrous cap formation. The mechanisms driving this synthetic transition remain unclear. Here we identify PRDM16, a gene linked to cardiovascular disease, as a critical transcriptional repressor of the synthetic SMC phenotype. PRDM16 expression declined during SMC modulation, and its deletion in mice induced a synthetic program across all SMC subtypes even without pathological stimuli. Under atherogenic conditions, PRDM16 deficiency resulted in the formation of fibroproliferative plaques with more synthetic SMCs and fewer foam cells. Conversely, enforced PRDM16 expression suppressed SMC migration, proliferation and fibrosis. Mechanistically, PRDM16 occupied chromatin and suppressed activating marks at synthetic loci. These findings establish PRDM16 as a gatekeeper of SMC fate and reveal its role in shaping atherosclerotic plaque composition.
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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.