Do biomarkers matter? Cardiovascular risk stratification in Asian patients with metabolic dysfunction-associated steatotic liver disease in the era of fibrosis-centric assessment

Figure 1 Conceptual framework linking biomarker domains to cardiovascular risk in metabolic dysfunction-associated steatotic liver disease. Metabolic indices (uric acid/high-density lipoprotein ratio, triglyceride-glucose, and triglyceride/high-density lipoprotein-cholesterol) reflect upstream insulin resistance and visceral adiposity, driving hepatic steatosis and lipotoxicity. Inflammatory markers (high-sensitivity C-reactive protein and homeostatic model assessment of insulin resistance) contribute to hepatokine dysregulation and endothelial dysfunction, promoting atherogenesis. Fibrosis-related markers (fibrosis-4 index, steatosis-activity-fibrosis evaluation index, and Wisteria floribunda agglutinin-positive Mac-2 binding protein) capture cumulative metabolic-inflammatory injury and progressive liver fibrosis, which closely associates with vascular pathology. Cardiac biomarkers (N-terminal pro-B-type natriuretic peptide and troponins) reflect downstream myocardial stress and injury. These interconnected pathways culminate in coronary artery disease, carotid atherosclerosis, and heart failure susceptibility. UHR: Uric acid/high-density lipoprotein cholesterol ratio; TyG: Triglyceride-glucose; HDL-C: High-density lipoprotein-cholesterol; hs-CRP: High-sensitivity C-reactive protein; HOMA-IR: Homeostatic model assessment of insulin resistance; FIB-4: Fibrosis-4 index; SAFF: Steatosis-activity-fibrosis evaluation index; WFA+-M2BP: Wisteria floribunda agglutinin-positive Mac-2 binding protein; NT-proBNP: N-terminal pro-B-type natriuretic peptide.