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This theory speculates that aging is a consequence of the failure of several defensive mechanisms to respond to the reactive oxygen species (ROS)-induced damage, particularly at the mitochondria (Islam, 2017)

Ferroptosis has emerged as a key contributor to ALI pathogenesis [160]

Accordingly, the SARSCoV2 genome and its products potentially modulate HMRD at transcription, translation, and post-translational modification (PTM) levels of human metabolism

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