SLC7A3（溶质载体家族7成员3，Solute Carrier Family 7 Member 3）属于SLC7基因家族，该家族主要编码氨基酸转运蛋白，负责跨膜运输阳离子氨基酸（如精氨酸、赖氨酸和鸟氨酸）。SLC7家族分为两个亚类：CAT（阳离子氨基酸转运蛋白）和LAT（L型氨基酸转运蛋白），SLC7A3属于CAT亚类，其表达产物是一种钠离子非依赖性的阳离子氨基酸转运蛋白，主要在中枢神经系统（如大脑皮层、海马体和下丘脑）以及外周组织（如肾脏和肠道）中表达，功能上参与精氨酸等阳离子的摄取，影响一氧化氮（NO）合成、多胺代谢和神经递质平衡。SLC7A3的突变可能导致氨基酸转运功能障碍，例如精氨酸缺乏会减少NO生成，影响血管舒张和神经信号传导，与神经系统疾病（如癫痫、精神分裂症）或心血管疾病潜在相关。若该基因过表达，可能增加细胞对精氨酸的摄取，导致NO过量引发氧化应激或炎症；而表达降低则可能限制精氨酸供应，影响蛋白质合成和免疫功能。SLC7A3所在的SLC7家族共性为通过形成异二聚体（通常与SLC3蛋白结合）实现膜定位和功能，且多数成员依赖溶质浓度梯度进行转运。目前关于SLC7A3的研究较少，其病理机制尚待深入探索。

该基因编码的溶质载体家族7编码的蛋白质的一个成员是钠依赖性阳离子氨基酸转运。在多个备选的成绩单剪接结果编码相同的蛋白质。[由RefSeq的，2010年5月提供]

SLC7A3, a member of the solute carrier family 7 (SLC7), encodes a sodium-independent transporter for cationic amino acids, specifically belonging to the cationic amino acid transporter (CAT) subfamily. This protein facilitates the bidirectional exchange of basic amino acids such as arginine, lysine, and ornithine across the plasma membrane, a process that is mechanistically dependent on the formation of a functional heterodimer with an SLC3 accessory subunit to ensure proper membrane localization and transport activity. Expressed predominantly in the central nervous system—including the cerebral cortex, hippocampus, and hypothalamus—as well as in peripheral tissues like the kidney and intestine, SLC7A3 plays a critical role in maintaining cellular amino acid homeostasis, thereby influencing downstream metabolic pathways including nitric oxide (NO) synthesis, polyamine metabolism, and neurotransmitter balance. Since arginine is the essential substrate for NO production, dysregulation of SLC7A3-mediated arginine uptake can have profound physiological consequences; for instance, reduced transporter activity may limit arginine availability, potentially impairing vascular relaxation, protein synthesis, and immune function, while contributing to neurological conditions such as epilepsy or schizophrenia through disrupted neural signaling. Conversely, overexpression or hyperactivity of SLC7A3 could lead to excessive arginine accumulation and subsequent overproduction of NO, which may trigger oxidative stress and inflammatory responses. Although the specific pathogenic mechanisms associated with SLC7A3 mutations are still being elucidated, its function in modulating cationic amino acid flux positions it as a key regulator in cardiovascular health, neurobiology, and systemic metabolic stability.

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