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Abstract
Introduction: Non-alcoholic fatty liver disease (NAFLD) represents the most prevalent chronic liver condition worldwide, affecting approximately 25–30% of the global adult population (Younossi et al., 2016). The disease encompasses a spectrum ranging from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, and ultimately cirrhosis. In recent years, the nomenclature has evolved to metabolic dysfunction-associated steatotic liver disease (MASLD), reflecting its deep interconnection with systemic metabolic disturbances (Rinella et al., 2023). Beyond hepatic manifestations, NAFLD has emerged as an independent risk factor for cardiovascular disease (CVD), which constitutes the leading cause of mortality in NAFLD patients (Targher et al., 2021). The pathophysiological mechanisms linking NAFLD to CVD include chronic systemic inflammation, oxidative stress, endothelial dysfunction, atherogenic dyslipidemia, and insulin resistance. These processes are mediated by a complex network of cytokines, adipokines, and hepatokines that create a pro-atherogenic milieu extending far beyond the liver parenchyma (Byrne & Targher, 2015).
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