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, pain sensation, and potentially other neurological functions. Genetic models, such as KO and CKO mouse models, have been crucial in understanding its functions [2].

In cardiac research, Scn10a-short, a transcript from an intronic enhancer-promoter complex in cardiomyocytes of the atria, sinoatrial node, and ventricular conduction system, was identified. Disrupting the mouse intronic enhancer using CRISPR/Cas9 led to reduced cardiac Scn10a-short expression, decreased cardiac sodium current in atrial cardiomyocytes, atrial conduction slowing, and arrhythmia [1].

In pain-related studies, complete loss-of-function or knockout (KO) of Scn10a in rodent models decreased sensitivity to various pain stimuli [2].

In conclusion, Scn10a plays essential roles in cardiac conduction and pain perception. The KO/CKO mouse models have significantly contributed to understanding its role in cardiac arrhythmias and pain-related diseases, providing insights into potential therapeutic targets for these conditions.