Slc38a2, also known as SNAT2 (Sodium-coupled Neutral Amino Acid Transporter 2), is a key amino acid transporter. It is involved in the transport of neutral amino acids such as glutamine, proline, and alanine, playing a vital role in multiple metabolic pathways. This gene is essential for maintaining normal physiological functions including cell growth, immune response, and tissue development [1,2,4]. Genetic models like knockout (KO) mouse models have been crucial in understanding its functions.

In mice, placenta-specific Slc38a2 knockdown causes fetal growth restriction (FGR), reducing near-term fetal and placental weight, fetal viability, and placental amino acid uptake [2]. In the renal medulla, Slc38a2-knockout mice exhibit increased medullary ferroptosis following water restriction, indicating its role in protecting renal medullary collecting duct cells from hyperosmolarity-induced ferroptosis via the mTORC1 signalling pathway [3]. In bone, genetic ablation of SLC38A2 using Prrx1Cre in mice leads to decreased bone mass due to reduced osteoblast numbers and activity [4].

In conclusion, Slc38a2 is essential for normal development and physiological function across multiple tissues. Studies using KO/CKO mouse models have revealed its critical roles in fetal growth, renal protection, and bone mass accrual. These findings provide potential therapeutic targets for diseases such as FGR and highlight the importance of Slc38a2 in maintaining tissue homeostasis [2,3,4].