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The main molecular mechanisms involved in the modulation of eryptosis studied to date, including intracellular calcium levels, ceramide, ROS, NO, changes in cellular energy metabolism, PS externalization, ion channel regulation, Fas-mediated signaling pathways, kinase-associated, and caspases activation, among others represent potential targets for inducing or inhibiting erythrocyte death
The development of an optimal therapy is, however, complicated by certain side effects, including the possibility of post-treatment hypothyroidism and recurrence of hyperthyroidism following an initial successful treatment
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