Glo1, also known as Glyoxalase I, is a cytosolic protein expressed in all mammalian cells. Its main function is the detoxification of methylglyoxal (MG), a potent precursor of advanced glycation end-products (AGEs), and it is involved in the cellular glycolysis pathway [3,4]. By regulating MG, Glo1 impacts various biological processes and is associated with multiple diseases, highlighting its biological importance [1].

Modulation of Glo1 activity has been shown to regulate anxiety-like behavior and seizure-susceptibility in mice, suggesting it as a novel target for neuropsychiatric and anti-epileptic drug development [1]. In hepatocellular carcinoma (HCC), Glo1 is overexpressed, activates the cell cycle pathway, and promotes cell proliferation and migration, making it a promising therapeutic target [2]. In glioma, high Glo1 expression is correlated with poor prognosis and enhances tumor cell proliferation, migration, and invasion [4]. In Escherichia coli, Glo1 contributes to drug resistance by inducing PER-type of extended-spectrum β-lactamases [5]. In human skeletal muscle, loss of NAMPT and SIRT2 attenuates Glo1 expression and activity [6]. In melanoma, genomic Glo1 deletion modulates TXNIP expression, glucose metabolism, and redox homeostasis while accelerating tumor growth [7]. In bladder cancer, miR-205-3p suppresses cancer progression via Glo1-mediated P38/ERK activation [8]. In HCC, Glo1 genetic amplification is associated with cell proliferation and survival, and interfering Glo1 expression inhibits tumor growth [9]. In a Chinese population, Glo1 SNPs are associated with gestational diabetes mellitus susceptibility [10].

In conclusion, Glo1 plays essential roles in multiple biological processes and diseases. Through various in vivo and in vitro models, its functions in neuropsychiatric disorders, cancers, bacterial drug resistance, and diabetes-related conditions have been revealed. These findings provide valuable insights into disease mechanisms and potential therapeutic strategies targeting Glo1.