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MOTS-c: the mitochondrial fat burner MOTS-c stands alone in this list because of its mechanism

The knockout of -Synuclein only increased the number of dopamine neurons which suggested that the loss of synucleins does not produce parkinsonism

Because MOTS-c is naturally produced in response to exercise, and because it activates the same AMPK and mitochondrial biogenesis pathways that exercise training upregulates, combining exogenous MOTS-c with a structured exercise program creates a reinforcing signal that operates through the same biological channels

Myocardial steatosis impairs left ventricular diastolicsystolic coupling in healthy humans