Metabolic Dysfunction-Associated Steatohepatitis and Progression to Hepatocellular Carcinoma: A Literature Review

• Published in: Cancers Vol. 16; no. 6; p. 1214
• Main Authors: Ghazanfar, Haider, Javed, Nismat, Qasim, Abeer, Zacharia, George Sarin, Ghazanfar, Ali, Jyala, Abhilasha, Shehi, Elona, Patel, Harish
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 20.03.2024; MDPI
• Subjects: Adipose tissue; Apoptosis; Biomarkers; Cell growth; Development and progression; Diabetes mellitus (non-insulin dependent); Diet; Fatty acids; Fatty liver; Fibrosis; Gender; Genetic factors; Hepatocellular carcinoma; Hepatoma; Homeostasis; Inflammation; Insulin resistance; Kinases; Lipid metabolism; Lipids; Lipogenesis; Lipolysis; Literature reviews; Liver cancer; Liver cirrhosis; Liver diseases; Medical research; Medicine, Experimental; Metabolic syndrome; Mortality; Obesity; Oxidation; Oxidative stress; Pathogenesis; Physiological aspects; Review; Risk factors; Steatosis; Surveillance; Type 2 diabetes; Urbanization; United States > US; North America; pathogenesis; HCC; progression; risk factors; MASH
• ISSN: 2072-6694; 2072-6694
• DOI: 10.3390/cancers16061214

The prevalence of metabolic-associated fatty liver disease (MAFLD) is increasing globally due to factors such as urbanization, obesity, poor nutrition, sedentary lifestyles, healthcare accessibility, diagnostic advancements, and genetic influences. Research on MAFLD and HCC risk factors, pathogenesis, and biomarkers has been conducted through a narrative review of relevant studies, with a focus on PubMed and Web of Science databases and exclusion criteria based on article availability and language. Steatosis marks the early stage of MASH advancement, commonly associated with factors of metabolic syndrome such as obesity and type 2 diabetes. Various mechanisms, including heightened lipolysis, hepatic lipogenesis, and consumption of high-calorie diets, contribute to the accumulation of lipids in the liver. Insulin resistance is pivotal in the development of steatosis, as it leads to the release of free fatty acids from adipose tissue. Natural compounds hold promise in regulating lipid metabolism and inflammation to combat these conditions. Liver fibrosis serves as a significant predictor of MASH progression and HCC development, underscoring the need to target fibrosis in treatment approaches. Risk factors for MASH-associated HCC encompass advanced liver fibrosis, older age, male gender, metabolic syndrome, genetic predispositions, and dietary habits, emphasizing the requirement for efficient surveillance and diagnostic measures. Considering these factors, it is important for further studies to determine the biochemical impact of these risk factors in order to establish targeted therapies that can prevent the development of HCC or reduce progression of MASH, indirectly decreasing the risk of HCC.