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Other mechanistic insights include excessive autophagy driven by an imbalance in the ROS/PI3K/AKT/mTOR axis [102], genetic variations (e.g., SOD gene polymorphisms) that impair ROS elimination [103], and additional pathways such as mitophagy dysregulation [106], AKT pathway inactivation [100], and mt-lysosome axis failure [29]

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In gut-focused research the relevant neighbors are KPV and the BPC-157 / KPV / larazotide capsule preparation, where the shared endpoints are barrier integrity and inflammatory mediator expression rather than angiogenesis