Apoo, also known as apolipoprotein O and MIC26, is a constitutive protein of the mitochondrial cristae organizing system complex [1,2,3,4]. It plays crucial roles in mitochondrial structure and function, and is involved in lipid metabolism-related pathways [1,5]. Its overall biological importance lies in maintaining normal physiological functions of adipose tissue, macrophages, and heart, and is associated with various disease conditions. Genetic models like KO/CKO mouse models have been valuable in studying its functions [1,2].

In adipocytes, Apoo-knockout (ApooACKO) mice showed increased adiposity, BAT dysfunction and whitening, reduced non-shivering thermogenesis, and blunted responses to cold stimuli [1]. Apoo deficiency disrupted mitochondrial structure in brown adipocytes, impaired oxidative phosphorylation, and induced a shift from oxidative to glycolytic metabolism, increasing lipogenic enzyme levels and BAT whitening [1].

In macrophages, macrophage-specific Apoo knockout (MIC26LysM) mice had smaller atherosclerotic lesions and necrotic core, and the loss of Apoo increased efferocytosis [2].

In global Apoo-knockout (Apoo-/ -) mice, Apoo depletion aggravated diet-induced obesity and elevated plasma cholesterol levels, and affected cholesterol metabolism independent of LDLR and APOE [5].

In conclusion, Apoo is essential for maintaining normal mitochondrial structure and function in multiple cell types. Through gene-knockout mouse models, its roles in obesity-related adipose tissue changes, atherosclerosis, and cholesterol metabolism have been revealed. These findings suggest Apoo could be a potential therapeutic target for obesity and atherosclerosis [1,2,5].