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(2018) showed MOTS-c translocates to the nucleus under metabolic stress, directly regulating adaptive nuclear gene expression a unique mechanism for a mitochondrially encoded peptide (PMID: 29983246)

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The novelty of the present study includes ranking of a multitude of factors contributing to circulating TMAO levels and identification of kidney function as the top modifiable factor in a non-CKD population across the cardiometabolic disease spectrum