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[1] At the cellular level, the tendon work is genuinely mechanistic: in cultured rat tendon fibroblasts, BPC-157 accelerated cell outgrowth, improved survival under oxidative stress, and increased migration in a dose-dependent way, apparently through the FAKpaxillin pathway

Moreover, at moderate levels, ROS oxidatively modifies KEAP1, thereby activating the NRF2 pathway, which induces the transcription of antioxidant genes such as SOD2, GPX1, and HO-1, establishing a defense against oxidative stress in granulosa cells [236]