ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
Blood Milieu in Acute Myocardial Infarction Reprograms Human Macrophages for Trauma Repair.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- An exploratory study of high-throughput transcriptomic analysis reveals novel mRNA biomarkers for acute myocardial infarction using integrated methods.Scientific reports · 2025Article
- Protein carbamylation in atherosclerotic plaques correlates with uremia and disease progression, localizing predominantly to foam cells.Frontiers in immunology · 2025Article
- Identification of a gene network driving the attenuated response to lipopolysaccharide of monocytes from hypertensive coronary artery disease patients.Frontiers in immunology · 2024Article
- Blood Milieu in Acute Myocardial Infarction Reprograms Human Macrophages for Trauma Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Culture density influences the functional phenotype of human macrophages.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 3 countries.
Funding
Abstract
Acute myocardial infarction (AMI) is accompanied by a systemic trauma response that impacts the whole body, including blood. This study addresses whether macrophages, key players in trauma repair, sense and respond to these changes. For this, healthy human monocyte-derived macrophages are exposed to 20% human AMI (n = 50) or control (n = 20) serum and analyzed by transcriptional and multiparameter functional screening followed by network-guided data interpretation and drug repurposing. Results are validated in an independent cohort at functional level (n = 47 AMI, n = 25 control) and in a public dataset. AMI serum exposure results in an overt AMI signature, enriched in debris cleaning, mitosis, and immune pathways. Moreover, gene networks associated with AMI and with poor clinical prognosis in AMI are identified. Network-guided drug screening on the latter unveils prostaglandin E2 (PGE2) signaling as target for clinical intervention in detrimental macrophage imprinting during AMI trauma healing. The results demonstrate pronounced context-induced macrophage reprogramming by the AMI systemic environment, to a degree decisive for patient prognosis. This offers new opportunities for targeted intervention and optimized cardiovascular disease risk management.
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Registered trials
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