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Further information on research design is available in the Reporting Summary linked to this article

S2CID 8837202

The attending physicians reported the outcome of the ICU patients as either dead or discharge

Excessive ROS disrupt the oxidation-antioxidant balance, activate inflammatory cell signals, and induce endothelial cell dysfunction through mitochondria-mediated apoptosis, promoting vascular smooth muscle cell proliferation, interfering with nitric oxide synthesis, and delaying endothelial repair, thereby accelerating atherosclerosis development (Tullio et al., 2013