ArticleInternational journal of molecular sciences2024
Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction.
Article in International journal of molecular sciences, 2024. 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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Who cites it
6 citing papers in PubMed.
- Spiny Mice Show a Profibrotic Epicardial Mesothelial Response to Hypoxic Injury Comparable to C57BL/6 Mice.Biomolecules · 2026Article
- Pericardial Inflammatory Mediators in Patients Undergoing Cardiac Surgery: Towards a Biomarker-Informed Clinical Practice.Reviews in cardiovascular medicine · 2026Review
- Plasma exosomal hsa-miR-339-5p is associated with NOD-like receptor family CARD domain-containing 5 in heart failure with reduced ejection fraction.Scientific reports · 2026Article
- Beyond cardiac fibroblasts: research advances on understanding and targeting intercellular communication networks in cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- The Molecular Relationship Between SDF4 and Thiol/Disulfide Homeostasis and Cardiac Injury Markers in Serum and Pericardial Fluid of Patients Undergoing Open-Heart Surgery.Journal of clinical medicine · 2025Article
- Article
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Authors and funding
12 authors.
Funding
Abstract
Pericardial fluid (PF) has been suggested as a reservoir of molecular targets that can be modulated for efficient repair after myocardial infarction (MI). Here, we set out to address the content of this biofluid after MI, namely in terms of microRNAs (miRs) that are important modulators of the cardiac pathological response. PF was collected during coronary artery bypass grafting (CABG) from two MI cohorts, patients with non-ST-segment elevation MI (NSTEMI) and patients with ST-segment elevation MI (STEMI), and a control group composed of patients with stable angina and without previous history of MI. The PF miR content was analyzed by small RNA sequencing, and its biological effect was assessed on human cardiac fibroblasts. PF accumulates fibrotic and inflammatory molecules in STEMI patients, namely causing the soluble suppression of tumorigenicity 2 (ST-2), which inversely correlates with the left ventricle ejection fraction. Although the PF of the three patient groups induce similar levels of fibroblast-to-myofibroblast activation in vitro, RNA sequencing revealed that PF from STEMI patients is particularly enriched not only in pro-fibrotic miRs but also anti-fibrotic miRs. Among those, miR-22-3p was herein found to inhibit TGF-β-induced human cardiac fibroblast activation in vitro. PF constitutes an attractive source for screening diagnostic/prognostic miRs and for unveiling novel therapeutic targets in cardiac fibrosis.
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Registered trials
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