ArticleCureus2025
The Potential Role of Serum Tissue Inhibitor of Metalloproteinase-2 (TIMP-2) as a Biomarker of Fibrosis in Patients With Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD).
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundActivation of hepatic stellate cells (HSCs) in response to liver injury increases extracellular matrix (ECM) deposition and upregulation of tissue inhibitor of metalloproteinase-2 (TIMP-2), promoting fibrogenesis, a key feature of metabolic dysfunction-associated fatty liver disease (MAFLD). This study was conducted to determine the diagnostic potential of serum TIMP-2 levels in patients with MAFLD/nonalcoholic fatty liver disease (NAFLD).
methodsThis case-control study included 100 MAFLD patients and 100 healthy controls. Demographic profiling, ultrasonography, and FibroScan with controlled attenuation parameter (CAP) scoring were conducted. Serum TIMP-2 was quantified using enzyme-linked immunosorbent assay (ELISA), and routine biochemical parameters (liver function test, kidney function test, fasting plasma glucose, postprandial blood sugar, HbA1c, total cholesterol, triglycerides, and GGT) were assessed using fully automated chemistry analyzers. Receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic utility of TIMP-2.
resultsSerum TIMP-2 levels were significantly higher in MAFLD patients (p < 0.001) compared with controls. Serum TIMP-2 showed a significant positive correlation with ALT (rho = 0.569, p < 0.001), GGT (rho = 0.551, p < 0.001), fasting plasma insulin (rho = 0.562, p < 0.001), and FibroScan scores (r = 0.560, p < 0.001). ROC analysis yielded an AUC of 0.933 (95% CI: 0.889-0.963) with a TIMP-2 cut-off value of 8.909, showing a sensitivity of 91% and specificity of 99%.
conclusionSerum TIMP-2 levels are significantly elevated in MAFLD and show strong correlations with liver enzymes and CAP scores, suggesting a relationship with hepatic fat accumulation and liver injury. Additionally, associations with lipid levels, white blood cell count, and neutrophils imply a link to systemic inflammation and liver fibrosis, highlighting the promising role of TIMP-2 as a noninvasive, blood-based biomarker for early detection and monitoring of liver fibrosis. Further studies are needed to substantiate the diagnostic potential of serum TIMP-2 in MAFLD patients.
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