SLC25A17 deficiency is associated with peroxisomal dysfunction, and its altered expression is implicated in various cancers and bipolar disorder, though its precise mechanisms remain unknown.
Solute carrier family 25 (SLC25) is known to facilitate the transport of diverse metabolites across the mitochondrial and peroxisomal membranes. SLC25A17 is the only member of the SLC25 protein localized to peroxisomes; formerly known as PMP34, it also shares conserved sequence features with other SLC families. SLC25A17 was first described as an ATP transporter, but conflicting results regarding cofactor specificity in various experimental models obscure its precise function. Similarly, phenotypic differences between experimental models, such as mice and zebrafish, complicate the application of animal studies to humans. In particular, SLC25A17 deficiency is associated with peroxisomal dysfunction, and SLC25A17 expression is affected in various cancers and bipolar disorder, while the underlying molecular mechanisms remain unknown. Furthermore, it remains unclear whether altered SLC25A17 expression is a cause or consequence of human disease. This review provides an overview on current knowledge of SLC25A17, focusing on its known functions and emerging roles in human diseases. This may also help future studies in understanding its metabolic significance and disease pathogenesis.
Chhetri et al. (2026) conducted a review in Peroxisome dysfunction, cancers, and bipolar disorder. SLC25A17 was evaluated. SLC25A17 deficiency is associated with peroxisomal dysfunction, and its altered expression is implicated in various cancers and bipolar disorder, though its precise mechanisms remain unknown.
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