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Understanding the underlying biological pathways associated with these disease modifiers, and how they influence fibrosis, may lead to new leads for therapeutic strategies

In an experimental model of induced fatigue bone damage, administration of CGRP or CGRP(837) increased reparative bone formation [74]

elegans FOXO, our findings suggest a conserved critical Ku70 role for FOXO function toward coordination of a survival program, regulated by the magnitude of oxidative damage

This effect may be attributed to its antioxidative properties, including the increase in SOD, CAT activity, and GSH levels in the hippocampus of diabetic rats, and the inhibition of ROS production in SH-SY5H cells treated with high glucose

doi:10.21037/tau-20-592