ArticleJournal of cardiovascular translational research2024
Short-term S100A8/A9 Blockade Promotes Cardiac Neovascularization after Myocardial Infarction.
Article in Journal of cardiovascular translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- CKD disrupts cardiac energy metabolism and aggravates cardiac inflammation, oxidative stress, and dysfunction post-infarction.Cardiovascular research · 2026Article
- S100A8/A9 and S100A12 Proteins and Macrophage Polarization: Therapeutic Targets in Atherosclerosis.Biomolecules · 2026Review
- Targeting S100A8/A9: a molecular gateway to oral inflammation, microglial activation and neuroinflammation.Frontiers in immunology · 2026Review
- Infant Viability in Severe Preeclampsia: Management Strategies and the Potential Role of Calprotectin-A Narrative Review.Children (Basel, Switzerland) · 2025Review
- Exploring the Relevance of S100A8 and S100A9 Proteins in Preeclampsia: A Narrative Review.International journal of molecular sciences · 2025Review
- Identification of neutrophil extracellular traps-related genes for the diagnosis of acute myocardial infarction based on bioinformatics and experimental verification.Journal of inflammation (London, England) · 2025Article
- Proposed Novel Heart Failure Biomarkers and Their Association with Length of Hospital Stay and Mortality: A Retrospective Observational Pilot Study.Diagnostics (Basel, Switzerland) · 2025Article
- The alarmin tandem: unraveling the complex effect of S100A8/A9 - from atherosclerosis to cardiac arrhythmias.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute-phase inhibition of the pro-inflammatory alarmin S100A8/A9 improves cardiac function post-myocardial infarction (MI), but the mechanisms underlying the long-term benefits of this short-term treatment remain to be elucidated. Here, we assessed the effects of S100A8/A9 blockade with the small-molecule inhibitor ABR-238901 on myocardial neovascularization in mice with induced MI. The treatment significantly reduced S100A9 and increased neovascularization in the myocardium, assessed by CD31 staining. Proteomic analysis by mass-spectrometry showed strong myocardial upregulation of the pro-angiogenic proteins filamin A (~ 10-fold) and reticulon 4 (~ 5-fold), and downregulation of the anti-angiogenic proteins Ras homolog gene family member A (RhoA, ~ 4.7-fold), neutrophilic granule protein (Ngp, ~ 4.0-fold), and cathelicidin antimicrobial peptide (Camp, ~ 4.4-fold) versus controls. In-vitro, ABR-238901 protected against apoptosis induced by recombinant human S100A8/A9 in human umbilical vein endothelial cells (HUVECs). In conclusion, S100A8/A9 blockade promotes post-MI myocardial neovascularization by favorably modulating pro-angiogenic proteins in the myocardium and by inhibiting endothelial cell apoptosis.
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