Scn10a, encoding the neuronal voltage-gated sodium channel NaV1.8, is involved in various physiological and pathological processes. It has been associated with pathways related to cardiac electrophysiology and pain perception [1,2]. Genetic models, such as KO and CKO mouse models, are valuable tools for studying its functions.

In KO mouse models, disruption of the mouse intronic enhancer of Scn10a led to reduced cardiac Scn10a-short expression, decreased cardiac sodium current in atrial cardiomyocytes, atrial conduction slowing, and arrhythmia [1]. Complete loss-of-function or knockout of Scn10a in rodent models decreased sensitivity to various pain stimuli [2].

In conclusion, Scn10a plays a crucial role in cardiac conduction and pain perception. KO/CKO mouse models have revealed its importance in these areas, highlighting its significance in diseases such as atrial fibrillation, Brugada syndrome, and pain-related disorders [1,2].