Metabolic dysfunction-associated fatty liver disease: from basic research to clinical application

Yang, Rui‐Xu; Qian, Jin; Fan, Jian‐Gao

doi:10.1097/cm9.0000000000002136

Cited by 2 publications

(2 citation statements)

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“… 7 , 8 This is very true in most developed nations with a sedentary lifestyle, where the imbalance between caloric intake and caloric output is steadily increasing. 9 , 10 The advanced stage of MASLD with liver cirrhosis is non‐reversible, and liver transplantation is the only option of treatment. 11 However, due to the shortage of organs available for transplant and the associated complications and rejection after transplantation, alternative treatment methods are a requisite.…”

Section: Introductionmentioning

confidence: 99%

“…Metabolic syndrome and the associated insulin resistance, oxidative stress, lipid peroxidation and proinflammatory cytokines have significant contributions to the pathogenesis and progression of MASLD 7,8 . This is very true in most developed nations with a sedentary lifestyle, where the imbalance between caloric intake and caloric output is steadily increasing 9,10 . The advanced stage of MASLD with liver cirrhosis is non‐reversible, and liver transplantation is the only option of treatment 11 .…”

Section: Introductionmentioning

confidence: 99%

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Molecular pathogenesis of metabolic dysfunction‐associated steatotic liver disease, steatohepatitis, hepatic fibrosis and liver cirrhosis

Saito,

Tsuchishima,

Tsutsumi

et al. 2024

J Cellular Molecular Medi

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Metabolic dysfunction‐associated steatotic liver disease (MASLD) is characterized by intense deposition of fat globules in the hepatic parenchyma that could potentially progress to liver cirrhosis and hepatocellular carcinoma. Here, we evaluated a rat model to study the molecular pathogenesis of the spectrum of MASLD and to screen therapeutic agents. SHRSP5/Dmcr rats were fed a high‐fat and cholesterol (HFC) diet for a period of 12 weeks and evaluated for the development of steatosis (MASLD), steatohepatitis, fibrosis and cirrhosis. A group of animals were sacrificed at the end of the 4th, 6th, 8th and 12th weeks from the beginning of the experiment, along with the control rats that received normal diet. Blood and liver samples were collected for biochemical and histopathological evaluations. Immunohistochemical staining was performed for α‐SMA and Collagen Type I. Histopathological examinations demonstrated steatosis at the 4th week, steatohepatitis with progressive fibrosis at the 6th week, advanced fibrosis with bridging at the 8th week and cirrhosis at the 12th week. Biochemical markers and staining for α‐SMA and Collagen Type I demonstrated the progression of steatosis to steatohepatitis, hepatic fibrosis and liver cirrhosis in a stepwise manner. Control animals fed a normal diet did not show any biochemical or histopathological alterations. The results of the present study clearly demonstrated that the HFC diet‐induced model of steatosis, steatohepatitis, hepatic fibrosis and cirrhosis is a feasible, quick and appropriate animal model to study the molecular pathogenesis of the spectrum of MASLD and to screen potent therapeutic agents.

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