Ephx2, also known as soluble epoxide hydrolase 2, encodes an enzyme that hydrolyzes 11,12-epoxyeicosatrienoic acid (11,12-EET) to less active dihydroxyeicosatrienoic acids. The arachidonic acid metabolic pathway, in which Ephx2 is involved, participates in various physiological processes [1,2].

In muscle regeneration, deletion of Ephx2 accumulates 11,12-EET, which accelerates muscle regeneration and rejuvenates aged muscle by amplifying fibroblast growth factor signalling [1]. In isolated mouse hearts, cardiomyocyte-specific disruption of Ephx2 improves functional recovery after ischemia-reperfusion, while endothelial cell-specific disruption has no significant effect [3]. In colon cancer, EPHX2 acts as a tumor suppressor by promoting fatty acid degradation [4]. In hepatocellular carcinoma, down-regulation of EPHX2 is associated with disease development, and higher EPHX2 expression indicates a better prognosis [5]. In ulcerative colitis, inhibiting the STAT3-EPHX2 axis by a novel porphyrin derivative can alleviate the disease [6]. In IEC-6 cells, Ephx2 silencing attenuates hydrogen peroxide-induced oxidative damage [7].

In conclusion, Ephx2 plays important roles in multiple biological processes and disease conditions. Gene-knockout (KO) or conditional-knockout (CKO) mouse models have revealed its function in muscle regeneration, cardiac post-ischemic recovery, and cancer progression, among others. These studies contribute to understanding the mechanisms of related diseases and provide potential therapeutic targets.