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Key actions include: Activation of the folate-polyamine-AICAR pathway, triggering AMPK signaling independently of cellular energy depletion Enhanced glucose uptake in skeletal muscle via GLUT4 translocation, resembling insulin-responsive metabolic pathways Interaction with nuclear transcription factors to support antioxidant defense and control of inflammatory pathways Through these mechanisms, MOTS-c functions as a mitochondria-to-nucleus messenger, facilitating cellular adaptation to energy demands and oxidative stress

*Correspondence: Kazuyuki Fujihara, [email protected] Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers