Jiang Lab

My lab studies lipid and lipoprotein metabolism in liver cells and steatotic liver diseases where lipid metabolisms are altered by nutritional imbalance, metabolic derangement, or cellular dysfunction. 

Research Areas

Fatty Liver 


Steatotic liver disease, commonly known as "fatty liver", is the most common form of liver disease in most societies. Fatty liver usually develops in metabolic dysfunction and heavy alcohol consumption. In both metabolic dysfunction associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD), impairment in lipid and lipoprotein metabolism plays a critical role. Our lab aims to understand mechanisms underlying lipid and lipoprotein metabolism in healthy and diseased states and develop novel therapeutic strategies to treat ALD and MASLD. 

Learn more about our research

 

Z. Gordon Jiang

MD, PhD

Principal Investigator

Meet the Team

Latest News

Featured Publications

  • Amjad, Waseem, Zhenghui Jiang, and Michelle Lai. “Statin Use in Cirrhosis and Its Association With Incidence of Portal Vein Thrombosis.”. Journal of Gastroenterology and Hepatology 39, no. 5 (2024): 955-63. doi:10.1111/jgh.16495.
    Publisher's Version
    Publisher's Version

    BACKGROUND AND AIM: Statin use has shown a reduction in hepatic decompensation and portal hypertension. Its association with portal vein thrombosis (PVT) incidence is unknown. We aim to compare the incidence of PVT in patients with and without statin use.

    METHODS: We excluded patients with a history of hepatocellular cancer, liver transplants, Budd-Chiari syndrome, and intra-abdominal malignancies. Patients with cirrhosis were followed from their first hepatologist clinical encounter (January 1, 2016, to January 31, 2021) for 180 days to determine PVT incidence. We tested the association of statin use with PVT using 1:1 propensity score (PS) matching and Cox proportional hazard regression.

    RESULTS: We analyzed 2785 patients with cirrhosis (mean age:61.0 ± 12.3 years, 44.3% female, 63.8% White, mean MELD-Na score:11.7 ± 6.1, and statin use:23.1%). A total of 89 patients developed PVT during the follow-up, which was lower in patients with statin use as compared to no statin use (1.3% vs 3.8%, P = 0.001, unadjusted HR:0.28, 95% CI: 0.13-0.62, P = 0.001). After matching for demographics, comorbidities, and hepatic decompensation events, patients with statin use had a lower risk of developing PVT in 180-day follow-up as compared to those without statin use (HR:0.24, 95% CI: 0.10-0.55, P = 0.001). Subgroup analysis showed that statin use was associated with lower PVT incidence in non-NASH (HR: 0.20, 95% CI: 0.07-0.54, P = 0.002) and decompensated cirrhosis (HR: 0.12, 95% CI:0.03-0.53, P = 0.005) than no statin use.

    CONCLUSION: PVT incidence was lower in decompensated cirrhosis patients with statin use than in those with no statin use. However, this finding needs to be further tested in randomized control trials.

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