Pathophysiology of Clopidogrel in Ischemic Stroke, Role of Platelet microRNAs
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064165%3A_____%2F25%3A10503534" target="_blank" >RIV/00064165:_____/25:10503534 - isvavai.cz</a>
Alternative codes found
RIV/00216224:14740/25:00142673 RIV/61988987:17110/25:A2603DN8 RIV/00216208:11110/25:10503534
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=SQskMgDSf6" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=SQskMgDSf6</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.33549/physiolres.935617" target="_blank" >10.33549/physiolres.935617</a>
Alternative languages
Result language
angličtina
Original language name
Pathophysiology of Clopidogrel in Ischemic Stroke, Role of Platelet microRNAs
Original language description
Variation in response to clopidogrel represents a significant clinical challenge in patients with ischemic stroke. Genetic polymorphisms cytochrome P450 2C19 (CYP2C19) are a known cause of resistance to clopidogrel. Platelet microRNAs (miRNAs) can modulate the efficacy of antiplatelet therapy. This study focuses solely on clopidogrel because it is the most widely used alternative to aspirin in patients with aspirin intolerance or contraindications. Our aim was to investigate its pharmacogenomic and epigenetic modulation in a targeted and homogeneous cohort. CYP2C19 genotypes are commonly reported as *1/*1 (wild type), *1/*2 (intermediate metabolizer), *2/*2 (poor metabolizer) and *2/*3 (poor metabolizer). These denote the number and type of loss-of-function alleles that affect clopidogrel metabolism. Clopidogrel treatment is typically a component of broader secondary prevention strategies, including lifestyle modifications, statins, and control of blood pressure. Relevant bibliographic references have been added to support the background statements provided in the introduction and methodology. To evaluate the expression of selected platelet miRNAs (miR-126-3p, miR-19a-3p, miR-19b-3p, miR-22-3p, miR-185-5p) in patients with ischemic stroke in relation to the CYP2C19 genotype (*1/*1,*1/*2, *2/*2) during clopidogrel treatment. Seventy patients treated with clopidogrel (75 mg daily) were enrolled. Patients were genotyped for the CYP2C19 *2 and *3 alleles by real-time polymerase chain reaction (polymerase chain reaction (PCR)) and miRNA expression was measured in plasma. All abbreviations used throughout the manuscript have been defined at their first appearance for the sake of clarity. No significant differences in miRNA expression were found between the genotypic groups (p > 0.05). Patients with genotype *2/*2 (poor metabolizer) showed a trend towards higher levels of miR-126-3p and miR-185-5p (approximately 1.5 to 1.7 times) compared to *1/*1 (wild type). The clinical parameters did not differ significantly between the groups. Poor clopidogrel metabolizers can exhibit upregulation of some platelet miRNAs as a potential compensatory mechanism. This pilot study suggests a possible epigenetic modulation of the response to antiplatelet therapy through platelet miRNAs.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
—
Continuities
V - Vyzkumna aktivita podporovana z jinych verejnych zdroju
Others
Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Physiological Research
ISSN
0862-8408
e-ISSN
1802-9973
Volume of the periodical
74
Issue of the periodical within the volume
4
Country of publishing house
CZ - CZECH REPUBLIC
Number of pages
7
Pages from-to
669-675
UT code for WoS article
001568778000013
EID of the result in the Scopus database
2-s2.0-105015030552