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Abstract
Fanconi anaemia (FA) is a DNA-repair disorder that compresses multiple hallmarks of ageing into childhood and early adulthood.
- FA-specific DNA-repair failure may be linked to mitochondrial metabolism.
- Oxidative stress, inflammatory changes, and metabolic reprogramming are associated with genomic instability in FA.
- These factors could erode epigenetic integrity and compromise immune function.
- FA may serve as a model to study the sequence and interdependence of ageing hallmarks.
- Nutrigenomic mechanisms, such as vitamin D-dependent chromatin changes, may influence epigenetic states.
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