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It plays a role in the mechanical conduction of blood flow shear force and can prevent endothelial cell dysfunction [9, 31]
This is because injections of TB4 into the hearts of mice (both injured and uninjured) basically kick-started repair processes and made the epicardium (the outermost layer of the heart) behave as it does in embryonic development
In this sense, MOTS-c works as an endogenous exercise mimetic, triggering AMPK activation through the same molecular lever that exercise pulls, just from the inside [1]
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& Pinheiro-Franco, J
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