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Combined intestinal loss of PPAR// attenuates KD-driven intestinal stem cell expansion, proliferation and clonogenicity, whereas inhibition of downstream fatty acid oxidation through CPT1A loss limits adenoma formation specifically under KD, linking tumour initiation to fatty acid oxidation of dietary lipids rather than lipid accumulation

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These disturbances, often influenced by intricate genetic determinants, can trigger multiple forms of programmed death in dopaminergic neurons, among which ferroptosis plays a significant role (119, 124)

Meanwhile, Kastner et al

We refer the reader to section V.H

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