ArticleJACC. Basic to translational science2023
Micronized Acellular Matrix Biomaterial Leverages Eosinophils for Postinfarct Cardiac Repair.
Article in JACC. Basic to translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Immunogenicity and Integration of a Decellularized Extracellular Matrix-Based Scaffold for the Reconstruction of Human Foreskin: A Preclinical Animal Study.Bioengineering (Basel, Switzerland) · 2025Article
- Charting New Real Estate: Leveraging the Therapeutic Potential of the Pericardial Space.JACC. Basic to translational science · 2024Article
- Extracellular Matrix Biomaterial Therapy for Myocardial Infarction: New Delivery Route and Immunomodulatory Effects.JACC. Basic to translational science · 2023Article
- Granulocytes and their Involvement in the Foreign Body Response to Biomaterials and Tissue Repair.In vivo (Athens, Greece)Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After ischemic injury, immune cells mediate maladaptive cardiac remodeling. Extracellular matrix biomaterials may redirect inflammation toward repair. Pericardial fluid contains pro-reparative immune cells, potentially leverageable by biomaterials. Herein, we explore how pericardial delivery of a micronized extracellular matrix biomaterial affects cardiac healing. In noninfarcted mice, pericardial delivery increases pericardial and myocardial eosinophil counts. This response is sustained after myocardial infarction, stimulating an interleukin 4 rich milieu. Ultimately, the biomaterial improves postinfarct vascularization and cardiac function; and eosinophil-knockout negates these benefits. For the first time, to our knowledge, we demonstrate the therapeutic potential of pericardial biomaterial delivery and the eosinophil's critical role in biomaterial-mediated postinfarct repair.
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Registered trials
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