The Relationship Between The Expression Of LRP1, LDLR, And LOX1 Receptors With The Steatosis Index And Liver Stiffness In Patients With Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is a multifactorial condition characterized by complex interactions between metabolic dysfunction, lipid accumulation, inflammation, and progressive fibrosis. Molecular mechanisms underlying these processes increasingly highlight the role of receptor genes involved in lipid transport and oxidative stress regulation. The present study aimed to investigate the association between the expression levels of LRP1, LDLR, and LOX1 receptor genes and key morphometric and non-invasive indicators of hepatic involvement in NAFLD. A cohort of patients with varying degrees of steatosis and fibrosis underwent molecular-genetic analysis, elastographic assessment of liver stiffness (Young’s modulus), and evaluation of the Fatty Liver Index (FLI). The results demonstrated that decreased expression of LRP1 and LDLR was significantly associated with higher FLI values, indicating a potential contribution of impaired receptor-mediated lipid uptake to the amplification of hepatic steatosis. These findings may reflect reduced hepatic clearance of circulating lipoproteins and altered lipid handling within hepatocytes, promoting intracellular lipid overload. In contrast, LOX1 expression showed a weak but statistically significant positive correlation with liver stiffness measurements, suggesting that oxidative stress and oxLDL-mediated signaling may participate in the early development of fibrosis. LOX1-dependent pathways are known to activate pro-inflammatory cascades, endothelial dysfunction, and extracellular matrix remodeling—mechanisms that could influence fibrogenesis in NAFLD. Collectively, the obtained data indicate that alterations in the expression profiles of LRP1, LDLR, and LOX1 may serve as molecular indicators of steatosis severity and early fibrotic changes. These genes may represent promising biomarkers for identifying patients at risk of progressive liver injury and developing personalized therapeutic strategies aimed at modifying lipid metabolism and oxidative stress. Further studies with larger cohorts and longitudinal follow-up are required to clarify the causal relationships and determine their potential as predictive markers in clinical practice.

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