Congenital portosystemic shunts (CPSS) are rare circulatory malformations that divert portal venous blood away from the liver, leading to reduced hepatic development and compromised liver performance. Felines affected by CPSS commonly display neurological and systemic abnormalities typical of hepatic encephalopathy (HE), arising from excess ammonia, inflammation, and oxidative imbalance. Surgical correction of the anomaly generally restores portal perfusion, improves liver capacity, and eliminates clinical manifestations. Despite these known physiological improvements, hepatic gene regulation in cats with CPSS has not yet been characterized.
This pilot investigation assessed liver mRNA expression in genes involved in the urea pathway (CPS1, NAGS), angiogenic activity (VEGFR2, NPPA, NPR1, NPPC, NPR2, HIF1a), hepatic repair (SERPINB1, HGF, TGFβ), and metabolism (FGF21). Samples were obtained from 18 affected cats and compared with 10 control subjects. Expression levels of TGFβ, VEGFR2, HGF, FGF21, and CPS1 were markedly elevated in shunt-affected liver tissue. Animals that tolerated only partial vessel closure exhibited stronger expression of SERPINB1, HIF1a, and NPR2 relative to those capable of complete ligation. No meaningful associations were detected between gene transcription and pre-surgical plasma ammonia levels. These molecular changes differed sharply from the expression signatures reported in canine CPSS, implying that cats may utilize different adaptive pathways in hepatic regulation.
