Macrophage scavenger receptor 1 (MSR1) mediates the uptake of modified lipoproteins, leading to macrophage foam cell formation and promoting the development and progression of nonalcoholic steatohepatitis.
This review highlights the role of MSR1 in macrophage foaming and lipid accumulation, suggesting it as a key mechanism and potential therapeutic target in the progression of NASH.
Nonalcoholic steatohepatitis (NASH) is the progressive form of nonalcoholic fatty liver disease (NAFLD), and the dysregulation of lipid metabolism and oxidative stress are the typical features. Subsequent dyslipidemia and oxygen radical production may render the formation of modified lipids. Macrophage scavenger receptor 1 (MSR1) is responsible for the uptake of modified lipoprotein and is one of the key molecules in atherosclerosis. However, the unrestricted uptake of modified lipoproteins by MSR1 and the formation of cholesterol-rich foamy macrophages also can be observed in NASH patients and mouse models. In this review, we highlight the dysregulation of lipid metabolism and oxidative stress in NASH, the alteration of MSR1 expression in physiological and pathological conditions, the formation of modified lipoproteins, and the role of MSR1 on macrophage foaming and NASH development and progression.
Sheng et al. (2022) conducted a review in Nonalcoholic steatohepatitis (NASH). Macrophage scavenger receptor 1 (MSR1) was evaluated. Macrophage scavenger receptor 1 (MSR1) mediates the uptake of modified lipoproteins, leading to macrophage foam cell formation and promoting the development and progression of nonalcoholic steatohepatitis.