Alox8, also known as murine Alox15b, is a lipoxygenase that catalyzes the peroxidation of arachidonic acid at carbon-8 [1]. It oxygenates polyunsaturated fatty acids in S -chirality with specific reaction specificity, and is involved in the arachidonate metabolism pathway. This pathway is crucial for various biological processes, and Alox8's function is significant in regulating biological activities related to lipid peroxidation [1]. Mouse models have been valuable for studying Alox8's role.

In mouse models, Alox8 deficiency leads to impaired recovery from influenza infection in an age -dependent manner, as 6 -month -old Alox8-/-mice showed prolonged illness compared to wild -type mice, with differences in cytokine levels [3]. Also, deletion of Alox8 on mouse chromosome 11B3 (homologous to human ALOX15B on chromosome 17p) contributes to B -cell malignancy. Alox8 loss upregulates the cyclooxygenase pathway, increasing the oncometabolite prostaglandin E2, which prevents pre -B cell apoptosis and differentiation. Repressing Cox -2 impairs tumorigenesis driven by Alox8 loss [2]. Additionally, a 1 -month intermittent fasting regimen in a mouse traumatic brain injury model elevated protective genes and partly abolished the increase of Alox8 induced by TBI, alleviating ferroptosis -related cellular damage and improving cognitive function [4].

In conclusion, Alox8 plays essential roles in processes such as recovery from influenza infection, B -cell malignancy regulation, and neuronal ferroptosis and cognitive function after traumatic brain injury. Mouse models, especially those with Alox8 deficiency, have been instrumental in revealing these functions, contributing to our understanding of related disease mechanisms [2,3,4].