Emodin attenuates estrogen-deficient sarcopenia by suppressing CYP1B1 to restore CD36-driven fatty acid handling in muscle stem cells.

Sarcopenia is a progressive, estrogen-deficiency-related syndrome characterized by the loss of muscle mass and regenerative capacity, particularly in postmenopausal women. We identify Emodin, a natural anthraquinone compound, as a potent metabolic modulator capable of alleviating sarcopenia through the CYP1B1/CD36 axis. Bioinformatics analysis revealed CYP1B1 as a top-ranked target of Emodin. In ovariectomized mice, Emodin administration significantly restored grip strength, muscle fiber architecture, and redox homeostasis. Mechanistically, Emodin suppressed CYP1B1 expression, thereby enhancing CD36-mediated Fatty Acid Handling [1,2], and improving MuSC survival and differentiation under oxidative stress. Inhibition of CD36 abolished these protective effects. These findings demonstrate that Emodin modulates CD36-associated lipid handling in MuSCs and highlight the CYP1B1/CD36 axis as a promising target for therapeutic intervention in estrogen-deficient sarcopenia.