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Damluji AA, van Diepen S, Katz JN, Menon V, Tamis-Holland JE, Bakitas M, Cohen MG, Balsam LB, Chikwe J, on behalf of the American Heart Association Council on Clinical C, Council on Arteriosclerosis T, Vascular B, Council on Cardiovascular S, Anesthesia, Council on C and Stroke N (2021) Mechanical complications of acute myocardial infarction: a scientific statement from the American Heart Association

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

Low iron or suboptimal protein intake

the specific mechanisms governing mitochondrial LIP formation, its crosstalk with cytoplasmic LIP, and its unique contribution to ferroptosis (distinct from cytoplasmic iron overload) are largely unresolved