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Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F24%3A00136630" target="_blank" >RIV/00216224:14110/24:00136630 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.mdpi.com/1422-0067/25/15/8329" target="_blank" >https://www.mdpi.com/1422-0067/25/15/8329</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/ijms25158329" target="_blank" >10.3390/ijms25158329</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction

  • Original language description

    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-beta-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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30201 - Cardiac and Cardiovascular systems

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2024

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    International Journal of Molecular Sciences

  • ISSN

    1661-6596

  • e-ISSN

    1422-0067

  • Volume of the periodical

    25

  • Issue of the periodical within the volume

    15

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    18

  • Pages from-to

    1-18

  • UT code for WoS article

    001286931200001

  • EID of the result in the Scopus database

    2-s2.0-85201015928