Abstract
Myocardial infarction (MI) is one of the main causes of mortality worldwide. Stroke ranks as another frequent cause of death and the foremost cause of disability. Acute MI is one of the most profound expressions of coronary artery illness and continues to be a predominant source of morbidity and death globally, although significant advancements in prognosis have occurred over the last decade. Importantly, MI elevates the risk of stroke in comparison to those without MI. Coronary heart disorder and certain subtypes of ischemic stroke have analogous pathogeneses, including inflammation and atherosclerosis progression. Moreover, MI may serve as a risk factor for stroke due to factors such as emboli following revascularization, atrial fibrillation associated with acute MI, or blood stasis in a partially functioning left ventricle. Moreover, stroke and MI share certain risk factors, including advancing age, diabetes, hypercholesterolemia, hypertension, and smoking. Oligonucleotides and decoy peptides are used to disrupt biological processes by imitating natural binding sites. Decoy peptides function as structural analogs of receptor proteins, attaching to ligands and obstructing their interaction with the real receptors. Conversely, oligonucleotide decoys are small DNA sequences that attach to transcription factors and prevent them from attaching to the sequences of their target genes. This review summarizes decoy-based research on MI and stroke.
| Original language | English |
|---|---|
| Article number | 115710 |
| Journal | Experimental Neurology |
| Volume | 401 |
| DOIs | |
| State | Published - Jul 2026 |
Keywords
- Atherosclerosis progression
- Coronary heart disorder
- Inflammation
- Myocardial infarction
- Oligonucleotides
- Target genes
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