Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by excessive accumulation of triglycerides and other lipids within liver cells and is closely associated with cardiovascular disease and metabolic syndrome. Very low-density lipoprotein (VLDL) is a lipoprotein synthesized and secreted by the liver and is primarily responsible for transporting triglycerides from the liver to peripheral tissues. Therefore, there is a strong association between MASLD and VLDL. Studies have found that excess production and abnormal metabolism of VLDL can lead to elevated blood triglyceride levels, which in turn promote fat deposition in the liver, leading to MASLD. During the pathophysiological process of MASLD, adipokines and inflammatory mediators secreted by adipose tissue can affect the metabolic network of the liver, further aggravating VLDL metabolic disorders. This paper reviews the effects of VLDL synthesis and metabolism on the development of MASLD, including the changes in VLDL structure and composition, the biosynthesis of VLDL, and the mechanism of underlying VLDL-associated damage, in an attempt to elucidate the intricate crosstalk between MASLD and VLDL, in order to provide new perspectives and methods for the prevention and treatment of related diseases.