Quercetin's Potential in MASLD: Investigating the Role of Autophagy and Key Molecular Pathways in Liver Steatosis and Inflammation
Abstract
Metabolic dysfunction-associated fatty liver disease (MASLD) is a widespread liver disorder characterized by excessive fat accumulation in the liver, commonly associated with metabolic syndrome components such as obesity, diabetes, and dyslipidemia. With a global prevalence of up to 30%, MASLD is projected to affect over 100 million people in the U.S. and 20 million in Europe by 2030. The disease ranges from Steatotic Lived Disease (SLD) to more severe forms like metabolic dysfunction-associated steatohepatitis (MASH), which can progress to cirrhosis and hepatocellular carcinoma. Autophagy, a cellular process crucial for lipid metabolism and homeostasis, is often impaired in MASLD, leading to increased hepatic lipid accumulation and inflammation. Key autophagy-related proteins, such as Beclin1, LC3A, SQSTM1 (p62), CD36, and Perilipin 3, play significant roles in regulating this process. Disruption in these proteins contributes to the pathogenesis of MASLD. Quercetin, a natural polyphenolic flavonoid with antioxidant and anti-inflammatory properties, has promising results in mitigating MASLD. It may reduce hepatic lipid accumulation, improve mitochondrial function, and enhance autophagy. However, further research is needed to elucidate its mechanisms and validate its therapeutic potential in clinical settings. This underscores the need for continued investigation into autophagy and novel treatments for MASLD.
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