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Description
These findings suggest that pathological cardiac pressure overload induces NNT reverse functional mode to generate NADH at the expense of NADPH resulting in a high NADH/NAD + and reductive stress, further promoting ROS at complex I leading to oxidative injury and cell death (Fig
Life Sci 2021
Additionally, prolonged exposure to silver sulfide-coated nanoparticles in E
Int Biodeterior Biodegradation
The pathophysiological processes of I/R injuries are both systemic and local and can be divided into two phases
