ArticleCommunications biology2023
Quantitative proteomic landscape of unstable atherosclerosis identifies molecular signatures and therapeutic targets for plaque stabilization.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- S100A8/A9 and S100A12 Proteins and Macrophage Polarization: Therapeutic Targets in Atherosclerosis.Biomolecules · 2026Review
- T-cadherin deprivation in endothelial cells promotes vascular injury in Kawasaki disease through SOD2/ROS/NLRP3 pathway-mediated pyroptosis.Journal of molecular cell biology · 2026Article
- Clonal haematopoiesis of indeterminate potential and mortality in coronary artery disease.European heart journal · 2026Article
- Multimodal landscape of atherosclerotic plaques: A spatial omics approach with mass spectrometry imaging.Analytica chimica acta · 2025Review
- Single-cell RNA-sequencing reveals adventitial fibroblast alterations during mouse atherosclerosis.Atherosclerosis · 2025Article
- Brain‑heart axis: Neurostimulation techniques in ischemic heart disease (Review).International journal of molecular medicine · 2025Review
- Atherosclerotic Plaque Instability and Rupture: Recommended Mouse Models to Empower Clinically Relevant Discoveries, Diagnostics, and Therapeutics.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Current status and challenges of multi-omics research using animal models of atherosclerosis.Journal of molecular and cellular cardiology plus · 2025Review
- Annexin-A1 deficiency uncovers female-specific pathways in blood pressure control and cardiovascular remodeling in mice.Communications biology · 2025Article
- Unraveling the proteomic signatures of coronary artery disease and hypercholesterolemia.Biomolecules & biomedicine · 2025Article
- Polymeric Nanomaterials for Atherosclerosis Diagnosis and Treatment.Polymer science & technology (Washington, D.C.) · 2025Review
- Redox Mechanisms Driving Skin Fibroblast-to-Myofibroblast Differentiation.Antioxidants (Basel, Switzerland) · 2025Article
- Proteomic analysis of carotid artery plaques with and without vulnerable features on magnetic resonance angiography with vessel wall imaging: a pilot study.JVS-vascular science · 2025Article
- Identification of Protein Networks and Biological Pathways Driving the Progression of Atherosclerosis in Human Carotid Arteries Through Mass Spectrometry-Based Proteomics.International journal of molecular sciences · 2024Article
- A near-complete assembly of the Houttuynia cordata genome provides insights into the regulatory mechanism of flavonoid biosynthesis in Yuxingcao.Plant communications · 2024Article
- Novel formylpeptide receptor 1/2 agonist limits hypertension-induced cardiovascular damage.Cardiovascular research · 2024Article
- Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction.Current issues in molecular biology · 2024Review
- Effects of vitamin D signaling in cardiovascular disease: centrality of macrophage polarization.Frontiers in cardiovascular medicine · 2024Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerotic plaque rupture leading to myocardial infarction is a major global health burden. Applying the tandem stenosis (TS) mouse model, which distinctively exhibits the characteristics of human plaque instability/rupture, we use quantitative proteomics to understand and directly compare unstable and stable atherosclerosis. Our data highlight the disparate natures and define unique protein signatures of unstable and stable atherosclerosis. Key proteins and pathway networks are identified such as the innate immune system, and neutrophil degranulation. The latter includes calprotectin S100A8/A9, which we validate in mouse and human unstable plaques, and we demonstrate the plaque-stabilizing effects of its inhibition. Overall, we provide critical insights into the unique proteomic landscape of unstable atherosclerosis (as distinct from stable atherosclerosis and vascular tissue). We further establish the TS model as a reliable preclinical tool for the discovery and testing of plaque-stabilizing drugs. Finally, we provide a knowledge resource defining unstable atherosclerosis that will facilitate the identification and validation of long-sought-after therapeutic targets and drugs for plaque stabilization.
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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.