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These results suggest that GLP-1/exendin-4 might compensate for the alterations in AMPK, activity produced either by oscillations in glucose levels or by pathologies such as obesity or episodes of hyperinsulinemia (Figure 5, 6)

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elucidated the upregulation of GPX3 in MI and delineated its candidacy as a prospective target for heart regeneration therapy through an integrative approach encompassing transcriptomic and proteomic analyses [79]

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