A Nutrigenomic View on the Premature-Aging Disease Fanconi Anemia.
Eunike VelleuerCarsten CarlbergPublished in: Nutrients (2024)
Fanconi anemia, a rare disorder with an incidence of 1 in 300,000, is caused by mutations in FANC genes, which affect the repair of DNA interstrand crosslinks. The disease is characterized by congenital malformations, bone marrow failure within the first decade of life, and recurrent squamous cell carcinomas of the oral cavity, esophagus, and anogenital regions starting around age 20. In this review, we propose that Fanconi anemia should be considered a premature-aging syndrome. Interestingly, the onset and severity of the life-limiting clinical features of Fanconi anemia can be influenced by lifestyle choices, such as a healthy diet and physical activity. These factors shape the epigenetic status of at-risk cell types and enhance the competence of the immune system through nutritional signaling. Fanconi anemia may serve as a model for understanding the aging process in the general population, addressing research gaps in its clinical presentation and suggesting prevention strategies. Additionally, we will discuss how the balance of genetic and environmental risk factors-affecting both cancer onset and the speed of aging-is interlinked with signal transduction by dietary molecules. The underlying nutrigenomic principles will offer guidance for healthy aging in individuals with Fanconi anemia as well as for the general population.
Keyphrases
- iron deficiency
- chronic kidney disease
- physical activity
- squamous cell
- bone marrow
- gene expression
- metabolic syndrome
- cardiovascular disease
- mesenchymal stem cells
- genome wide
- weight loss
- stem cells
- risk factors
- depressive symptoms
- single molecule
- cell therapy
- transcription factor
- papillary thyroid
- high grade
- case report
- human health
- copy number