Hepatic Mechanisms of Myocardial Infarction: A New Perspective in Metabolic Dysfunction‐Associated Fatty Liver Disease

Myocardial infarction is a major disease that seriously jeopardizes human health, and patients with comorbid metabolic disorders usually have a faster progression and worse prognosis. The presence of metabolic dysfunction-associated fatty liver disease not only exacerbates insulin resistance and metabolic imbalance but also contributes to the progression of myocardial infarction in a multifaceted and multifaceted manner through interactions with peripheral adipose tissue, the intestinal microbiota, and epigenetic alterations, as well as "direct communication" between the heart and the liver. Both physiologically and pathologically, it is of interest to note that cross-organ "direct communication" between the heart and the liver can occur in a variety of ways through a variety of means, including extracellular vesicles. In recent years, a variety of drugs with cardiovascular benefits have been found to treat metabolic dysfunction-associated fatty liver disease, and the mechanisms are worth exploring. It is important to explore the hepatic mechanism of myocardial infarction from a new perspective of metabolic dysfunction-associated fatty liver disease, which is centered on the imbalance of metabolic homeostasis and the process of heart-hepatic interorgan communication, for the prevention and treatment of cardiovascular diseases.