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Given the experimental evidence mentioned above, investigating new proeryptotic and antieryptotic molecules is essential for expanding our understanding of the cellular mechanisms underlying the programmed death of erythrocytes and for opening new avenues in the study of pathologies associated with eryptosis

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Through the inhibition of phosphoinositide 3-kinase (PI3K), 3-MA disrupts the formation of autophagosomes, thereby impeding the initiation of the autophagic process

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