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As mentioned above, FLS migration and invasion can lead to tissue destruction and accelerated joint damage in individuals with RA

Clinical translation in the future will depend on thorough microbiome profiling, life-cycle sustainability evaluations, and progressive regulatory frameworks

Similarly, inhibition of CD38 in aged mice boosted NAD + levels, improving exercise capacity, but in this case, no significant changes in mitochondrial biogenesis-related genes were observed 138

This damage can result in mutations within oncogenes such as RAS and MYC, as well as tumor suppressor genes like p53 and PTEN, thereby fostering genomic instability and malignant transformation [31, 32]