Slc25a5, also known as solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 5 or ANT2, is a critical inner mitochondrial membrane protein. It functions as a transporter for metabolites at the inner mitochondrial membrane and is involved in processes like oxidative phosphorylation and ATP production. It participates in pathways such as PINK1-PRKN-dependent mitophagy, and also has implications in adipogenesis through modulating the ERK signaling pathway [2,3].

In colon cancer, Slc25a5 was downregulated, and its upregulation was related to better overall survival. High Slc25a5 expression was an independent prognostic factor for patients after surgical treatment. It attenuated cell proliferation, upregulated programmed cell death-related signatures, and inhibited the MAPK signaling pathway [1].

In diabetes-induced osteopenia, BK channels regulated Slc25a5-mediated mitophagy in osteoblasts [2].

In adipogenesis, depletion of Slc25a5 in OP9 cells led to suppressed adipogenesis-related gene expression, reduced triglyceride accumulation, and inhibited PPARγ protein expression [3].

In neuroblastoma, high expression of Slc25a5 predicted poor patient prognosis, and inhibiting this transporter reduced cell viability [4].

In summary, Slc25a5 plays essential roles in multiple biological processes and disease conditions. Its dysregulation is associated with colon cancer, diabetes-induced osteopenia, adipogenesis, and neuroblastoma. Studies on Slc25a5, including those using gene-knockout or other loss-of-function models, have provided insights into its functions and its potential as a therapeutic target in these diseases.