The utility of STRIATIN as a novel diagnostic marker in cirrhosis.

BACKGROUND

Endothelial dysfunction and endothelial nitric oxide synthase (eNOS) mediated reduction in nitric oxide (NO) bioavailability are pivotal in the pathogenesis of portal hypertension (PHT) associated with liver cirrhosis. Striatin, a scaffolding protein that regulates eNOS activation, may play a crucial but unexplored role in this context. This study aimed to investigate hepatic striatin expression and its association with eNOS in cirrhosis, assess systemic striatin concentrations in cirrhotic patients, and evaluate its potential as a diagnostic biomarker for PHT.

MATERIALS AND

METHODS

A case-control study was conducted including 40 cirrhotic patients and 40 age- and sex-matched healthy controls. Hepatic striatin and phosphorylccated eNOS (peNOS) expressions were determined by Western blotting. Serum striatin and cyclic guanosine monophosphate (cGMP) concentrations were measured using ELISA, and biochemical parameters were analyzed using a Beckman Coulter AU 680 autoanalyzer.

RESULTS

Serum striatin levels were significantly lower in cirrhotic patients than in controls (6.86 ± 1.7 vs. 10.9 ± 1.7 ng/ml; P < 0.0001). Conversely, serum cGMP levels were significantly higher in cirrhotic patients (10.90 ± 2.8 vs. 5.19 ± 2.3 pmol/ml; P < 0.0001), with no correlation observed between striatin and cGMP concentrations. Hepatic striatin expression was markedly reduced in cirrhotic livers and positively correlated with peNOS levels. Receiver operating characteristic (ROC) analysis demonstrated that serum striatin had superior diagnostic accuracy compared with cGMP for distinguishing cirrhotic patients from controls.

CONCLUSIONS

Both systemic and hepatic striatin levels are significantly reduced in cirrhosis, suggesting a potential role of striatin downregulation in endothelial dysfunction and PHT. Striatin may serve as a promising diagnostic biomarker for cirrhotic patients with PHT. Further studies are warranted to elucidate the therapeutic potential of the striatin-eNOS-NO signaling axis in advanced cirrhosis.