ArticleiScience2026
Integrin-linked kinase promotes hepatic fat accumulation via F-actin stabilization-dependent CD36 plasma membrane localization.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Increased hepatic lipid accumulation occurs in high-fat diet (HFD)-induced insulin resistance. Integrin-linked kinase (ILK) contributes to HFD-induced hepatic insulin resistance by increasing hepatic triglyceride content. How ILK promotes HFD-induced hepatic fatty acid accumulation is underexplored. ILK favors the formation of F-actin bundling and is upregulated following HFD. Moreover, the fatty acid transporter CD36 localizes to membrane ruffles rich in F-actin following HFD. Thus, we investigated whether ILK-mediated F-actin stabilization and liver fatty acid uptake are mechanistically linked. HFD-fed mice lacking ILK in hepatocytes have reduced hepatic F-actin abundance, CD36 plasma membrane localization, and intracellular lipid accumulation. ILK-null cells treated with the F-actin stabilizer jasplakinolide increased cortical F-actin polymerization, plasma membrane-associated CD36, and intracellular lipid uptake. CD36 inhibition reduced lipid uptake in jasplakinolide-treated ILK-null cells, confirming that F-actin-induced CD36 plasma membrane localization promotes lipid accumulation. Thus, ILK regulates intracellular lipid transport by linking CD36 to an F-actin-rich cytoskeleton.
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