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We demonstrate mechanistically the need for increased mitochondrial function, facilitated by mTORPGC1-mediated mitochondrial biogenesis, to support rebalancing of pyrimidines via UCK2 to support cellular survival in the face of continued 5FU treatment

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Future research should leverage advanced techniques like spatial multi-omics analysis and patient-derived organoids/assembloids to directly validate how iron accumulation drives senescence and fibrosis in this disease, which is crucial for translating this hypothesis into clinical practice