Introduction: Intravenous dexmedetomidine may influence cardiomyocyte biology through effects on apoptosis, inflammation, oxidative stress, and mitochondrial function, with possible relevance in perioperative and critical care settings. However, available evidence remains heterogeneous and translationally uncertain. This study aims to systematically evaluate its cellular effects on cardiomyocytes and clarify their clinical relevance.

Material and methods: This systematic review followed PRISMA guidelines, searched PubMed, Scopus, Web of Science, and Embase without time restriction using Boolean operators, and included original English studies on intravenous dexmedetomidine and cardiomyocyte biology. Study selection and quality assessment were performed independently by two reviewers, and key methodological and outcome data were extracted from each article.

Results: Dexmedetomidine consistently exerts direct cardiomyocyte-protective effects by attenuating apoptosis, oxidative stress, and inflammation across various stress models. Key mechanisms include activation of antioxidant pathways, enhanced autophagic flux via adrenergic signaling, and epigenetic regulation of anti-inflammatory axes. Additionally, it modulates electrophysiological properties by suppressing sodium and calcium currents, demonstrating a pleiotropic capacity to preserve cellular homeostasis and functional integrity.

Conclusion: Dexmedetomidine functions as a potent pleiotropic modulator of cardiomyocyte biology, providing robust protection against ischemic and oxygen-related stress. Beyond its sedative properties, it directly influences survival signaling, redox balance, and electrophysiology through diverse molecular pathways. These findings underscore its potential as a targeted cardioprotective agent, necessitating further clinical exploration to translate these cellular benefits into perioperative patient care.