Dear Colleagues,

In a cell, homeostasis is maintained when the cell has the capacity, and sustained ability, to compensate for biochemical events that are challenged by a lack or excess of biosynthetic precursors or enzymatic products. Many of these biochemical events rely on the sustained abundance of simple precursors and the enzymes responsible for their conversion.  In many cases, these conversions also require the contribution of coenzymes (e.g., ThPP, FAD, NAD, CoA, PLP, biotin, folate, cobalamin, SAM, and coQ) in addition to cofactors such as metals and ATP. These coenzymes and cofactors are not only central to metabolism, but many are also directly involved in the orchestration of a plethora of protein-driven signaling events that consume them (e.g., NAD+ (protein ADP-ribosylation and deacylation), acyl-coA (protein acylation), and SAM (nucleic acid and histone methylation)). Since these mediators are consumed, they can be readily depleted upon cellular response to intra and extracellular signaling events and their abundance can vary greatly over a cell cycle with physiological consequences that are slowly becoming better understood, such as loss of homeostasis.

The biosynthetic pathways that cells have available to maintain coenzymes levels can vary greatly across the phyla, organism and cell type. In mammals, most coenzymes are derived from vitamins but what constitutes a vitamin for some organisms is endogenously produced by others and this symbiosis is slowly emerging as being central to human health. Overall, these coenzymes are prone to regulation, via the abundance of their respective precursors as well as by genetic and epigenetic regulation. Crucially, these biosynthetic pathways often rely on the abundance of multiple coenzymes. For example, the interconversion of folate-derived coenzymes requires FAD and NADPH, while NAD de novo biosynthesis from tryptophan requires PLP and ThPP. As such, the interdependence of coenzyme biosynthesis should not be underestimated, as the reduction in one coenzyme form can affect the generation of another coenzyme whose abundance affects widely different cellular processes. Recently, the bioavailability of coenzymes and regulation of their biosynthetic pathways have become targets of drug development, either with the view to boosting their abundance for the improvement of cellular function or to inhibit their formation to promote cell death.  We seek manuscript submissions for a special edition to highlight the interconnectivity and interdependence of coenzymes and their metabolic pathways in the maintenance of cellular homeostasis.

Prof. Dr. Marie Migaud
Guest Editor

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• coenzymes
• cofactor
• homeostasis
• Acyl-CoA (ThDP, FAD……)
• FMN
• folate
• biotin
• metals/ATP
• metabolic pathways