Preventing a protein called AGTR2 from going about its work — either by removing it through genetic engineering or by using pharmacological agents to silence it — improved lung function in mouse models of cystic fibrosis (CF), a study reports.

Earlier work linking this protein to pulmonary disease in CF patients, including those of young age, was further supported by this study.

The research, “AGTR2 absence or antagonism prevents cystic fibrosis pulmonary manifestations,” was published in the Journal of Cystic Fibrosis.

Genetic differences unrelated to CFTR gene mutations — the cause of CF — are associated with lung disease in these patients. Specifically, a genome-wide association study (GWAS) in more 6,000 individuals spotted variants (differences) related to the severity of CF pulmonary disease that included the type 2 angiotensin II receptor (AGTR2) gene. [That study was published in 2015.]