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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]

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)

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