Cysltr1, also known as Cysteinyl leukotriene receptor 1, is a key receptor through which cysteinyl leukotrienes (CysLTs), a group of eicosanoids, regulate the pathogenesis of various human diseases [6]. It is involved in multiple signaling pathways such as NF-κB, ERK1/2, and may be associated with G protein-coupled signaling cascade [1,5,4]. Cysltr1 is of great biological importance in processes like allergic reactions, cell proliferation, and senescence [5,4]. Genetic models, such as the generation of CysLTR1 L118F mutant mice, have been used to study its functions [6].

In psoriasis, CYSLTR1 is increased in psoriatic skin lesions. CYSLTR1 knockout (KO) mice induced with imiquimod (IMQ) showed improvement in psoriasis-related parameters like PASI scores, serum IL-17A/F levels, and reduced Th1 and Th17 cells in the spleen and skin compared to wild-type mice. This indicates that Cysltr1 plays a role in psoriasis development [1].

In uveal melanoma (UM), CYSLTR1 is upregulated and its pharmacological blockage reduces the growth and metabolic activity of UM cell lines, suggesting its role in UM progression [2].

In diabetes-induced aortic and testicular injury, montelukast, a CysLTR1 antagonist, protects against injury by reducing levels of CysLTR1, TLR4, NF-κB and related inflammatory markers, and stimulating autophagy [3].

In adenoid hypertrophy, CYSLT1 expression is higher in patients compared to controls and is positively associated with disease severity, and may contribute to its progression by activating ERK1/2 [5].

In conclusion, Cysltr1 is crucial in various disease-related biological processes. The use of KO mouse models has revealed its roles in psoriasis, uveal melanoma, diabetes-related complications, and adenoid hypertrophy. These findings help in understanding the disease mechanisms and may provide potential therapeutic targets for these diseases.