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Using several AMPK activators, including BI-9774 freely available via #opnMe, the authors show: - In FBXL4-deficient cells, AMPK activation blocks mitophagy despite continued BNIP3/NIX accumulation, indicating inhibition at the level of autophagy initiation via ULK1 regulation - Mitochondrial protein levels, mtDNA content, and respiratory capacity are restored to near wild-type levels - The rescued mitochondria are functional, with improved oxygen consumption across respiratory states - Similar rescue is observed in patient-derived fibroblasts carrying pathogenic FBXL4 variants - In a chemically induced mouse model of MTDPS13, AMPK activation reduced excessive mitophagy in liver and brain Mechanistically, the study reveals a context-dependent role for AMPK, which inhibits BNIP3/NIX-mediated degradation of functional mitochondria while preserving pathways that remove damaged organelles

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However, after oral administration of hydergine, subjects who were again exposed to the same conditions achieved significantly better results [150]