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Oxidative stress worsens mitochondrial damage The elevated production of ROS has been shown to induce depolarization of the mitochondrial membrane potential (m) and the subsequent opening of the mitochondrial permeability transition pore (mPTP) [76, 77]

In a study examining the microbiota in children prior to the development to T1D (children were negative for anti-islet antibodies, however, they possessed the predisposing HLA genotypes), several bacterial taxa correlated with the development of anti-islet antibodies found in T1D children

From bench to bedside: platelet biomimetic nanoparticles as a promising carriers for personalized drug delivery

These findings further validate the extraordinary antioxidant capacity of G/D-CuP, emphasizing its promise for use in wound repair

Mitochondrial dysfunction contributes to excessive production of mitochondrial ROS and mutations in mtDNA, further exacerbating oxidative stress