Introduction: NASH is a major driver of HCC, yet mechanisms linking inflammation to NASH-HCC remain unclear. Cholesterol has emerged as a key pathogenic factor promoting this progression, motivating targeted therapies (1). Here, we develop an apoA-I-decorated liposomal platform co-delivering simvastatin and sorafenib for NASH-HCC treatment. This system inhibits cholesterol biosynthesis and induces ferroptosis via suppression of SLC7A11 and GPX4. Ferroptosis further triggers immunogenic cell death, enhances antitumor immunity with aPD-L1 therapy, and reduces tumor burden while alleviating lipid accumulation and inflammation. 翻译
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Learning Objectives:
Understand the role of cholesterol metabolism in the progression of NASH-HCC
Explain the design and targeting mechanism of apoA-I-decorated liposomal nanoplatforms for drug delivery in HCC
