
-   The liver was found to be the main LCN-2 source during infection or post-partial hepatectomy (PHx). Dramatic increase in mRNA expression in liver as well as circulating LCN-2 in plasma was observed mouse model of PHx [PMID: 25234944].
-   In ob/ob mice, administration of a single ethanol dose led to liver injury and increased the hepatic mRNA expression of LCN2, among other chemokines and neutrophil-related proteins [PMID: 37019681].
-   Patients with chronic hepatitis C virus infection showed increased hepatic LCN-2 mRNA expression correlating with the stage of liver injury [PMID: 22553397].
-   LCN2 mRNA expression was significantly repressed by PPARalpha activation in human liver slices [PMID: 26449539].
-   RORalpha activation reduced the transcriptional expression of Lcn2 in mice with diethylnitrosamine-induced acute liver injury [PMID: 31409825].
-   LCN2 expression was found to be upregulated in various types of liver tumors, including AOX-/-, ciprofibrate-induced, and DENA-induced hepatocellular carcinomas in mouse models [PMID: 12771043].
-   Dietary vitamin D modulated Lcn2 expression in rat ICC tissues and human specimens, with a decrease in expression being noted in cells treated with active vitamin D [PMID: 24939880].
