24(S),25-Epoxycholesterol, Endogenous cholesterol metabolite

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Liver X receptors known as LXR alpha and LXR beta are nuclear receptors that regulate cholesterol fatty acid and glucose metabolism. They also have alternate names like NR1H3 (LXR alpha) and NR1H2 (LXR beta). LXRs function as transcription factors activated by endogenous metabolites like oxysterols. LXR alpha is highly expressed in liver adipose tissue kidney and macrophages while LXR beta shows a more ubiquitous distribution. The mass of LXR alpha is approximately 50 kDa and both play important roles in lipid homeostasis.

Biological function summary

LXR receptors regulate genes involved in lipid metabolism cholesterol efflux and inflammation. They form permissive heterodimers with Retinoid X Receptors (RXRs) to influence metabolic and inflammatory pathways. LXRs enhance the expression of transporter proteins such as ATP-binding cassette (ABC) transporters supporting cholesterol efflux and maintaining lipid balance. LXR activation leads to suppression of inflammatory gene expression in macrophages highlighting its role in immune response modulation.

Pathways

LXRs play a significant role in the reverse cholesterol transport and lipid metabolism pathways. They interact intimately with proteins like ABC transporters and the sterol regulatory element-binding protein 1c (SREBP-1c) to mediate lipid homeostasis. LXRs influence the liver and adipose tissue lipid management and their activity affects cholesterol clearance and storage. Their role intertwines with other nuclear receptors emphasizing their importance in maintaining metabolic harmony.

Dysregulation of LXR activity links to atherosclerosis and metabolic syndrome. Dysregulated LXR signaling can lead to the accumulation of cholesterol in blood vessels enhancing atherosclerosis risk. Furthermore alterations in LXR-mediated lipid metabolism contribute to metabolic syndrome impacting glucose and fatty acid balance. In a disease context LXRs connect with proteins like RXRs and SREBPs suggesting potential targets for therapeutic intervention in lipid-related disorders.