ADAM33, also known as A Disintegrin And Metalloprotease Domain 33, is a gene with significant implications in respiratory-related biological processes. It may play a role in airway remodeling, smooth muscle cell proliferation, and angiogenesis [1,4,6]. Its restricted expression to mesenchymal cells suggests its involvement in the structural airway components of asthma [6].

Multiple studies have explored ADAM33 polymorphisms in relation to diseases. Meta-analyses have found that certain polymorphisms such as T2, Q1, F + 1, and AA genotype of T + 1 in ADAM33 are associated with asthma risk, especially in Asian populations [2,8]. ADAM33 T1, T2, V4, and Q-1 polymorphisms may also be risk factors for allergic rhinitis [3]. Additionally, the F + 1 polymorphism in ADAM33 gene is associated with an increased risk of chronic obstructive pulmonary disease (COPD) in the Asian population [7]. In terms of functional studies, silencing of ADAM33 in human aortic smooth muscle cells inhibits cell migration and regulates cytokine secretion via the PI3K/AKT/mTOR pathway, contributing to the understanding of airway vascular remodeling in asthma [5].

In conclusion, ADAM33 is a gene of great importance in respiratory diseases like asthma, allergic rhinitis, and COPD. Its polymorphisms are closely associated with disease susceptibility, and functional studies, such as gene silencing experiments, have provided insights into its role in airway-related biological processes. These findings enhance our understanding of the disease mechanisms and may potentially lead to new therapeutic strategies targeting ADAM33 in these respiratory conditions.