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This cascade results in irreversible proteotoxic stress, ultimately leading to cardiomyocyte death [74]

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Subcutaneous administration in normal and metabolically dysregulated mice significantly inhibits NNMT activity in metabolically active tissues (adipose, liver, muscle), increases systemic NAD+ levels, enhances mitochondrial function, and improves energy metabolism

2 These include: A ME/CFS-like phenotype with post-exertional malaise and impaired bioenergetics A dysautonomia/POTS-dominant presentation A mast celldriven inflammatory phenotype Persistent cardiopulmonary injury This heterogeneity explains why a single treatment approach fails

The treatment with FLC showed a noteworthy different behaviour between the two resistant strains