Exosomes and non-coding RNAs: Exploring their roles in human myocardial dysfunction
Jazyk angličtina Země Francie Médium print-electronic
Typ dokumentu časopisecké články, přehledy
PubMed
39827809
DOI
10.1016/j.biopha.2025.117853
PII: S0753-3322(25)00047-2
Knihovny.cz E-zdroje
- Klíčová slova
- Bioengineering, Cardiomyopathies, Exosomes, Myocardial dysfunction, Non-coding RNAs,
- MeSH
- exozómy * metabolismus genetika MeSH
- fibróza MeSH
- kardiomyopatie * genetika metabolismus patofyziologie terapie MeSH
- lidé MeSH
- myokard * metabolismus patologie MeSH
- nekódující RNA * metabolismus genetika MeSH
- signální transdukce MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- nekódující RNA * MeSH
Myocardial dysfunction, characterized by impaired cardiac muscle function, arises from diverse etiologies, including coronary artery disease, myocardial infarction, cardiomyopathies, hypertension, and valvular heart disease. Recent advancements have highlighted the roles of exosomes and non-coding RNAs in the pathophysiology of myocardial dysfunction. Exosomes are small extracellular vesicles released by cardiac and other cells that facilitate intercellular communication through their molecular cargo, including ncRNAs. ncRNAs are known to play critical roles in gene regulation through diverse mechanisms, impacting oxidative stress, fibrosis, and other factors associated with myocardial dysfunction. Dysregulation of these molecules correlates with disease progression, presenting opportunities for therapeutic interventions. This review explores the mechanistic interplay between exosomes and ncRNAs, underscoring their potential as biomarkers and therapeutic agents in myocardial dysfunction. Emerging evidence supports the use of engineered exosomes and modified ncRNAs to enhance cardiac repair by targeting signaling pathways associated with fibrosis, apoptosis, and angiogenesis. Despite promising preclinical results, delivery, stability, and immunogenicity challenges remain. Further research is needed to optimize clinical translation. Understanding these intricate mechanisms may drive the development of innovative strategies for diagnosing and treating myocardial dysfunction, ultimately improving patient outcomes.
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