Liver X receptor β (LXRβ) is a nuclear receptor activated by oxysterols that regulates cholesterol, lipid, and glucose homeostasis
[1][2][3]. Mechanistically, LXRβ modulates transcription of key lipogenic genes such as SREBP1c and FASN, independently of LXRα, thereby controlling cellular lipogenesis in mammalian tissues including adipocytes and mammary epithelial cells
[4][2]. In the immune system, LXRβ is essential for T cell fitness and the suppression of CD4
+ T cell senescence, which contributes to the maintenance of immune homeostasis and limits inflammatory bowel disease progression
[5][6]. In the central nervous system, LXRβ influences synaptic plasticity, neuroinflammation, and excitatory/inhibitory neurotransmission, demonstrating isoform-specific roles in hippocampal- and amygdala-dependent cognitive and anxiety-related behaviors
[7][8]. Compared with LXRα, LXRβ has less impact on macrophage-mediated cholesterol efflux, cardiac ischemia/reperfusion injury, and intestinal sterol transport, highlighting functional specialization between isoforms
[9][10][11][12]. Pharmacologically, LXRβ-selective agonists and antagonists have been developed to exploit these specific functions, enabling modulation of lipogenesis, glucose metabolism, and immune responses without eliciting LXRα-driven hepatic lipogenesis
[13][14][3]. Therefore, LXRβ serves as a distinct therapeutic target for metabolic, immune, and neurological research applications, with experimental utility in both cell-based and in vivo models
[13][15][2][6].