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These findings imply that TST and its isoforms may be involved in the progression of vascular endothelial damage caused by ROS, positioning TST as a potential biomarker and therapeutic target for the prevention and management of atherosclerosis and CKD [129]
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The virus disrupts mitochondrial homeostasis through loss of mitochondrial membrane potential (ΔΨm), mitochondrial permeability transition pore (MPTP) opening, and increased ROS release, which may promote SARS-CoV-2 replication [102]
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