Acsbg1, short for Acyl-CoA Synthetase Bubble Gum 1, is a gene involved in fatty acid metabolism. It is part of the ACSL family, facilitating the activation of long-chain fatty acids (LCFAs) and their integration into essential lipid species. This process supports vital functions like membrane formation, myelination, and energy production, and is crucial for maintaining lipid homeostasis in various biological systems [4,5].

Genetic deletion of Acsbg1 in mice causes mitochondrial dysfunction and dampens other metabolic pathways. In Treg cells, Acsbg1 is selectively expressed, and its deficiency impairs Treg cell homeostasis, leading to an inability to resolve lung inflammation [1]. In CD4+ T cells, Acsbg1 deficiency results in impaired TH17 and in vitro-induced Treg (iTreg) cell differentiation, exacerbating colitis in adoptive transfer models [3]. In a mouse model of obesity-accelerated breast cancer, breast cancer cells in obese animals upregulate Acsbg1 to promote creatine-dependent tumor progression [2]. In the context of X-linked adrenoleukodystrophy (XALD), an Acsbg1 knockout mouse model showed developmental and compositional changes in fatty acid levels in the brain, though it's unlikely that Acsbg1 directly contributes to XALD pathology [4,5]. In diabetic cardiomyopathy rat models, Acsbg1 expression is significantly increased in the model group compared to the control group, and it may be associated with fatty acid metabolism and affect the occurrence and progression of the disease through the lysosome [6].

In summary, Acsbg1 plays essential roles in lipid metabolism, immune cell homeostasis, and differentiation, as well as in disease-related processes such as obesity-driven breast cancer and diabetic cardiomyopathy. The use of Acsbg1 knockout mouse models has been instrumental in uncovering these functions, providing valuable insights into the underlying mechanisms of these biological processes and diseases.