Acute ischemic stroke (AIS) is a leading cause of long-term disability and death. The genetic, epigenetic, and molecular mechanisms underlying AIS in young adults require further investigation. Inflammatory pathways, such as the programmed death-ligand 1 (PD-L1) and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway, are implicated in promoting post-ischemic neuroinflammation and neuronal apoptosis. While miR-155 and miR-216a are mediators of inflammation, apoptosis, and tissue repair following AIS. This exploratory study aimed to analyze the expression of the JAK2/STAT3, miR-155, and miR-216a genes in young AIS patients (mean age: 39.4 ± 11.9 years) versus the healthy population (HP). Peripheral blood samples were collected, and gene and miRNA expressions were measured using quantitative real-time PCR. Our results showed that stroke patients exhibited overexpression of all genes (p < 0.001), except for miRNA-216a (p = 0.061), compared to HP. These findings suggest that JAK2, STAT3, and miR-155 could be potential biomarkers for patients with AIS.
Vidal-González et al. (Thu,) studied this question.
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