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Primarily, it is logical to consider caspase-8 as a possible molecular switch that determines the plasticity of cell death pathways in mature erythrocytes, since caspase-8 is a well-known cell fate-determining enzyme, regulating apoptosis, necroptosis, or pyroptosis depending on its own activation status and interactions with other components of the cell death machinery [129, 209]

This is not merely additive: the MOTS-c may amplify or extend the mitochondrial biogenesis signal beyond what training alone achieves, particularly in older adults whose endogenous MOTS-c response to exercise is blunted [2]

Rhee SG

(2020) 16:e9510