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 [5]. It is involved in signaling pathways such as NF-κB and ERK1/2, playing significant roles in inflammatory responses, cell proliferation, and autophagy [1,3,4]. Genetic models like the CysLTR1 L118F mutant mice have been used to study its function [5].

In psoriasis, CYSLTR1 antagonist montelukast reduces disease symptoms in imiquimod-induced mice, inhibits Th17 cell differentiation by regulating NF-κB signaling, and CYSLTR1 knockout (KO) mice show improvement in psoriasis-related parameters [1]. In uveal melanoma, pharmacological blockage of CYSLTR1 reduces cell growth and increases apoptosis [2]. In diabetes-induced aortic and testicular injury, montelukast, a CysLTR1 antagonist, ameliorates inflammation by affecting TLR4 and NF-κB pathways [3]. In adenoid hypertrophy, CYSLTR1 promotes disease progression by activating ERK1/2 [4].

In conclusion, Cysltr1 plays essential roles in inflammation, cell proliferation, and apoptosis, and is involved in diseases like psoriasis, uveal melanoma, diabetes-related complications, and adenoid hypertrophy. Studies using KO mouse models and antagonist treatments have significantly contributed to understanding its role in these disease conditions, providing potential therapeutic strategies for these diseases.