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While targeting glutamine pathwaysparticularly GLS1 and -KG metabolismpresents promising antifibrotic potential, the cell type-specific and compensatory mechanisms highlight the need for precise therapeutic strategies to effectively harness glutamine-targeted interventions in IPF (Fig

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The catch, as always, is that most of what's discussed is preclinical-cell work, animal studies, and mechanistic hypotheses that still need careful replication

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My MTHFR gene function is reduced by about 70% as I have one MTHFR C677T and one MTHFR A1298C polymorphism