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Already in the 90s, early studies identified key regulators of protein synthesis, such as S6K1 and 4E-BP1, to be responsive to AA sufficiency, thus linking AA to mTORC1 activation (Hara et al., 1998)

La mitocondria necesita grasa para generar energa, esta no puede entrar en forma de cidos grasos de cadena larga, se necesita un trasportador para estos cidos grasos y este es la carnitina

These findings align with prior studies indicating that AAA pathogenesis involves pronounced recruitment of innate and adaptive immune cells, contributing to tissue degradation and remodeling[42, 48]