ArticleCardiovascular research2022
Neutralization of S100A4 induces stabilization of atherosclerotic plaques: role of smooth muscle cells.
Article in Cardiovascular research, 2022. 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, 34 citations in OpenAlex.
- The role of Smoothelin-B in abdominal aortic aneurysm formation.Biochemistry and biophysics reports · 2026Article
- Gordonibacter-associated regulatory T cell dysfunction and S100A11-mediated neural impairment in Hirschsprung's disease: a microbiota-immune-neural axis.Cell & bioscience · 2026Article
- S100A4 triggeres the pyroptosis of vsmcs: association with mitochondrial damage, impaired mitophagy, and CaBiology direct · 2026Article
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Article
- Smooth muscle cells in atherosclerosis: essential but overlooked translational perspectives.European heart journal · 2025Review
- Atypical mesenchyme in congenital pulmonary airways malformation: a promising new focus.Respiratory research · 2025Article
- SCAP Interacts with Trim27 to Promote Vascular Neointimal Hyperplasia by Regulating the Stability and Ubiquitination of IκBα.Aging and disease · 2025Article
- Inhibition of S100A4 decreases neurotoxic astrocyte reactivity and attenuates neuropathic pain via the TLR4/NF-κB pathway in a rat model of spinal nerve ligation.The journal of headache and pain · 2025Article
- Targeting RAGE-signaling pathways in the repair of rotator-cuff injury.Molecular and cellular biochemistry · 2025Review
- Development of stem cell therapy for atherosclerosis.Molecular and cellular biochemistry · 2024Review
- Re-analysis of single-cell transcriptomics reveals a critical role of macrophage-like smooth muscle cells in advanced atherosclerotic plaque.Theranostics · 2024Article
- S100A4 Is a Key Facilitator of Thoracic Aortic Dissection.International journal of biological sciences · 2024Article
- Apelin is expressed in intimal smooth muscle cells and promotes their phenotypic transition.Scientific reports · 2023Article
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- iTRAQ Proteomics Identified the Potential Biomarkers of Coronary Artery Lesion in Kawasaki Disease and In Vitro Studies Demonstrated That S100A4 Treatment Made HCAECs More Susceptible to Neutrophil Infiltration.International journal of molecular sciences · 2022Article
- Single cell transcriptomics and TCR reconstruction reveal CD4 T cell response to MHC-II-restricted APOB epitope in human cardiovascular disease.Nature cardiovascular research · 2022Article
- Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsDuring atherosclerosis, smooth muscle cells (SMCs) accumulate in the intima where they switch from a contractile to a synthetic phenotype. From porcine coronary artery, we isolated spindle-shaped (S) SMCs exhibiting features of the contractile phenotype and rhomboid (R) SMCs typical of the synthetic phenotype. S100A4 was identified as a marker of R-SMCs in vitro and intimal SMCs, in pig and man. S100A4 exhibits intra- and extracellular functions. In this study, we investigated the role of extracellular S100A4 in SMC phenotypic transition. METHODS AND
resultsS-SMCs were treated with oligomeric recombinant S100A4 (oS100A4), which induced nuclear factor (NF)-κB activation. Treatment of S-SMCs with oS100A4 in combination with platelet-derived growth factor (PDGF)-BB induced a complete SMC transition towards a pro-inflammatory R-phenotype associated with NF-κB activation, through toll-like receptor-4. RNA sequencing of cells treated with oS100A4/PDGF-BB revealed a strong up-regulation of pro-inflammatory genes and enrichment of transcription factor binding sites essential for SMC phenotypic transition. In a mouse model of established atherosclerosis, neutralization of extracellular S100A4 decreased area of atherosclerotic lesions, necrotic core, and CD68 expression and increased α-smooth muscle actin and smooth muscle myosin heavy chain expression.
conclusionWe suggest that the neutralization of extracellular S100A4 promotes the stabilization of atherosclerotic plaques. Extracellular S100A4 could be a new target to influence the evolution of atherosclerotic plaques.
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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.