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Collectively, these observations highlight a convergent pathogenic mechanism in NDDs, in which mitochondrial quality control failure, through impaired mitophagy, defective protein import, and ROS-driven dysfunction, links mitochondrial damage, mtDNA-mediated inflammation, and protein aggregation [68,69,70,71,72,73]

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The thinkings that BPC-157 can accelerate cellular signalling and fibroblast recruitment, while TB-500 handles the vascular supply and cytoskeletal remodelling necessary for sustained tissue regeneration