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摘要
<jats:p>Hepatocellular carcinoma (<jats:styled-content style="fixed-case">HCC</jats:styled-content>) is the sixth most frequent neoplasm and the second leading cause of cancer‐related deaths worldwide. Nonalcoholic fatty liver disease (<jats:styled-content style="fixed-case">NAFLD</jats:styled-content>), a common disorder in obese people, has been identified as an important risk factor for <jats:styled-content style="fixed-case">HCC</jats:styled-content>. Following the increasing prevalence of obesity, it is expected that the contribution of <jats:styled-content style="fixed-case">NAFLD</jats:styled-content> to <jats:styled-content style="fixed-case">HCC</jats:styled-content>'s incidence worldwide will grow. Recently, a number of studies have been published, which help us better understand cellular and molecular mechanisms of how <jats:styled-content style="fixed-case">NAFLD</jats:styled-content> promotes hepatocarcinogensis. Inflammatory cytokines, <jats:styled-content style="fixed-case">ER</jats:styled-content> stress and circadian dysregulation, which mediate hepatocyte injury and <jats:styled-content style="fixed-case">NAFLD</jats:styled-content> progression, have been identified to promote malignant transformation of hepatocytes. Besides these ‘intrinsic’ effects, lipid dysregulation dramatically affects the liver local microenvironment. The reshaped immune environment has also been found to contribute to the <jats:styled-content style="fixed-case">NAFLD</jats:styled-content>‐mediated hepatocarcinogenesis. This review explores recent findings of both ‘intrinsic’ effects on hepatocytes and the role of the local environment in <jats:styled-content style="fixed-case">NAFLD</jats:styled-content>‐promoted <jats:styled-content style="fixed-case">HCC</jats:styled-content> development.</jats:p>
- 出版日期2018-2
