Scnn1b, encoding the β subunit of the epithelial sodium channel (ENaC), plays a crucial role in sodium reabsorption. ENaC is involved in maintaining electrolyte balance and fluid homeostasis, with its activity influencing multiple physiological processes. Genetic models, such as knockout mouse models, are valuable tools for studying Scnn1b's functions [3,4,6].

In human lung fibroblasts, silencing Scnn1b enhanced cell proliferation and decreased migration, while also inhibiting collagen deposition-related proteins, suggesting its involvement in the development of acute respiratory distress syndrome (ARDS) [1]. In Scnn1b-transgenic BALB/c mice, overexpression of ENaC in the lungs led to increased sodium absorption and lung pathology similar to cystic fibrosis (CF). These mice had higher bacterial burdens and slower clearance of Pseudomonas aeruginosa infections, indicating its role in CF-related lung infections [2].

Mutations in Scnn1b are associated with Liddle syndrome, an autosomal-dominant form of monogenic hypertension. In a family with Liddle syndrome, a frameshift mutation in Scnn1b was identified, characterized by early-onset hypertension and hypokalemia [3]. Also, in a study of an adolescent with suspected Liddle syndrome, a recurrent Scnn1b mutation was detected, highlighting the importance of genetic screening in early-onset hypertensive patients [4].

In colorectal cancer, SCNN1B functions as a tumor suppressor, suppressing cell proliferation, inducing apoptosis, and cell cycle arrest, and suppressing cell migration both in vitro and in vivo. It does so by suppressing active c-Raf and the MAPK signaling cascade [5].

In conclusion, Scnn1b is essential for maintaining normal physiological functions related to sodium balance. Model-based research, especially with mouse models, has revealed its significance in diseases like ARDS, CF-related lung infections, Liddle syndrome, and colorectal cancer. Understanding Scnn1b's functions provides insights into the pathophysiology of these diseases and may guide the development of targeted therapies.