ArticleJournal of physiology and biochemistry2026
Irisin promotes lipid clearance through the CD81-integrin-FAK axis in steatotic hepatocytes.
Article in Journal of physiology and biochemistry, 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
Irisin, an exercise-induced myokine, regulates metabolic homeostasis, but its receptor mechanisms in metabolic dysfunction-associated steatotic liver disease (MASLD) remain unclear. This study investigates the role of the co-receptor CD81 in modulating irisin signaling and intrahepatic lipid homeostasis. Clinical correlations were analyzed in 88 bariatric surgery patients and liver biopsy cohorts (n = 62). In vitro steatosis models included Clone-9 rat hepatocytes, primary mouse hepatocytes, and human HepG2 and Huh-7 cells treated with fatty acids and recombinant irisin. Receptor interactions and downstream signaling were evaluated using co-immunoprecipitation, RT-qPCR, Western blotting, subcellular fractionation, and lipid staining. Serum irisin positively correlated with BMI and steatosis grade, but inversely associated with triglycerides, fasting glucose, and HbA1c. Intrahepatic FNDC5/irisin and integrin β5 correlated with serum triglycerides, whereas membranous CD81 expression declined with advancing steatosis. Free fatty acids induced FNDC5/irisin and perilipins (Plin2/Plin5) while downregulating CD81. Co-immunoprecipitation confirmed physical interaction between CD81 and integrins αV/β5 subunits. CD81 overexpression enhanced irisin-induced focal adhesion kinase (FAK) phosphorylation, restricted PPARγ nuclear translocation, suppressed Plin2/Plin5 expression, and attenuated lipid accumulation. Conversely, FAK inhibition using BI 853520 or CD81 knockdown abrogated these protective anti-steatotic effects. In conclusion, CD81 serves as a functional co-receptor that physically associates with the integrin αV/β5 complex to amplify irisin-FAK signaling, restrict PPARγ nuclear transactivation, and suppress lipid droplet accumulation in cultured hepatocytes in vitro. These findings highlight the CD81-integrin-FAK axis as a potential candidate for further translational exploration in MASLD.
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