to the pathogenesis of AFLD. Asp binding to its receptor C5aR2 promotes the expression of cytochrome P450 family 2, subfamily E, polypeptide 1, which induces the production of ROS. The induced oxidative stress subsequently leads to the increased expression of glycine tRNA-derived fragments (Gly-tRFs). Gly-tRF antisense inhibitor treatment can prevent the development of AFLD by reducing fatty acid synthesis and increasing fatty acid oxidation through regulating the SIRT1 signaling pathway in ethanol-fed mice. This study bridges the knowledge gap between the complement system, oxidative stress, and steatosis through elucidating the role of Gly-tRFs in ALD [32].
