ArticleInternational journal of molecular sciences2022
Short-Term Blockade of Pro-Inflammatory Alarmin S100A9 Favorably Modulates Left Ventricle Proteome and Related Signaling Pathways Involved in Post-Myocardial Infarction Recovery.
Article in International journal of molecular sciences, 2022. 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, 14 citations in OpenAlex.
- Clinically validated immune-related gene markers and molecular subtypes in acute myocardial infarction revealed by peripheral blood transcriptomics.Frontiers in cardiovascular medicine · 2026Article
- Cardiac ATP production and contractility are favorably regulated by short-term S100A9 blockade after myocardial infarction.Journal of advanced research · 2025Article
- The alarmin tandem: unraveling the complex effect of S100A8/A9 - from atherosclerosis to cardiac arrhythmias.Frontiers in immunology · 2025Review
- Short-term S100A8/A9 Blockade Promotes Cardiac Neovascularization after Myocardial Infarction.Journal of cardiovascular translational research · 2024Article
- The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction.Current issues in molecular biology · 2024Review
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- S100a8/9 (S100 Calcium Binding Protein a8/9) Promotes Cardiac Hypertrophy Via Upregulation of FGF23 (Fibroblast Growth Factor 23) in Mice.Journal of the American Heart Association · 2024Article
- Cardiac Alarmins as Residual Risk Markers of Atherosclerosis under Hypolipidemic Therapy.International journal of molecular sciences · 2022Article
- Article
- S100A8∕A9 is a valuable biomarker and treatment target to detect and modulate neutrophil involvement in myocardial infarction.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Prognosis after myocardial infarction (MI) varies greatly depending on the extent of damaged area and the management of biological processes during recovery. Reportedly, the inhibition of the pro-inflammatory S100A9 reduces myocardial damage after MI. We hypothesize that a S100A9 blockade induces changes of major signaling pathways implicated in post-MI healing. Mass spectrometry-based proteomics and gene analyses of infarcted mice left ventricle were performed. The S100A9 blocker (ABR-23890) was given for 3 days after coronary ligation. At 3 and 7 days post-MI, ventricle samples were analyzed versus control and Sham-operated mice. Blockade of S100A9 modulated the expressed proteins involved in five biological processes:
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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.