Elucidating the Shared Pathophysiology Between Metabolic Dysfunction-Associated Steatotic Liver Disease and Cardiovascular Disease

Metabolic dysfunction-associated steatotic liver disease (MASLD), characterized by hepatic triglyceride accumulation exceeding 5% of liver volume, is a prevalent manifestation of metabolic syndrome. It frequently coexists with obesity, type 2 diabetes mellitus, and dyslipidemia, driven by underlying insulin resistance and metabolic dysregulation. Current understanding points to a complex interplay of genetic, environmental, and inflammatory factors influencing MASLD progression. This review aims to clarify the intricate shared pathophysiological links between MASLD and cardiovascular disease (CVD), which remains a leading cause of morbidity and mortality in MASLD patients, often surpassing liver-related complications.

This comprehensive review synthesized existing scientific literature to elucidate the complex pathophysiological interrelationship between Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Cardiovascular Disease (CVD). The authors systematically analyzed studies focusing on shared underlying mechanisms, including insulin resistance, atherogenic dyslipidemia, endothelial dysfunction, and chronic low-grade systemic inflammation. The methodology involved a critical evaluation of published research to construct a cohesive understanding of how MASLD directly impacts cardiac structure and function, beyond its established vascular effects, and how these conditions mutually exacerbate each other through shared metabolic pathways.

The review identified a robust and multifactorial interrelationship between MASLD and CVD, underpinned by several shared pathophysiological mechanisms. Key among these are insulin resistance, which drives both hepatic steatosis and systemic metabolic dysfunction, and atherogenic dyslipidemia, characterized by elevated triglycerides and low HDL cholesterol, contributing to atherosclerotic plaque formation. Furthermore, the review highlighted endothelial dysfunction as a critical link, where MASLD-induced inflammation and metabolic stress impair vascular integrity. > Chronic low-grade systemic inflammation emerged as a central driver, with inflammatory mediators originating from the steatotic liver contributing to systemic inflammation, thereby accelerating atherosclerosis and directly impacting cardiac function. The authors emphasized that MASLD not only contributes to traditional cardiovascular risk factors but also directly influences cardiac structure and function, suggesting a direct hepatocardiac axis. This comprehensive synthesis underscores that MASLD is not merely a comorbidity but an active participant in the pathogenesis of CVD.