ArticleFrontiers in pharmacology2025
MT2 receptor mediates melatonin-induced thermogenic program in human myoblasts: insights for circadian syndrome and diabesity treatment.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Melatonin is crucial for regulating circadian rhythms. Previous studies have demonstrated its ability to improve metabolic disorders, including obesity and associated diabetes (diabesity), in addition to its antioxidant, anti-inflammatory and anti-apoptotic properties. Recently, melatonin was shown to reduce obesity by increasing skeletal muscle (SKM) energy expenditure through non-shivering thermogenesis (NST). Small interfering RNAs (siRNAs) are powerful tools for inhibiting gene expression, enabling the analysis of gene functions and roles in molecular pathway activation. This study aimed to identify the receptor mediating melatonin's pharmacological actions in SKM NST. Methods: Bioinformatics and protein-protein interaction (PPI) analyses were conducted. To examine the role of the melatonin receptor 2 (MT2) encoded by Results: PPI analysis revealed Conclusion: Our findings confirm that MT2 plays a key role in melatonin-driven SERCA-SLN uncoupling and the activation of the thermogenic program in SKM
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