Cav3, also known as T-type, low-voltage activated calcium channels, play a crucial role in regulating neuronal excitability. They are involved in a wide variety of physiological functions, especially in the nervous system, contributing to sensory processing, sleep, and hormone and neurotransmitter release [1].

In pain research, Cav3.2, a major isoform, is highly expressed in nonpeptidergic and peptidergic nociceptive neurons. In different pain models, its expression and activity increase in the spinal dorsal horn and dorsal root ganglia neurons. Genetic knockout of Cav3.2 reduces scratching behaviors in an atopic dermatitis-like mouse model, indicating its role in acute and chronic itch and inflammation [3].

In non-alcoholic fatty liver disease (NAFLD) mouse models, Cav3.2 knockout improves hepatic steatosis, liver injury, and metabolic syndrome by inhibiting oxidative stress, inflammation, and hepatocyte apoptosis [2].

In cerebral ischemia/reperfusion injury models, Cav3.2 knockout reduces infarct volume, brain water content, and alleviates neurological dysfunction by attenuating oxidative stress, inflammatory response, and neuronal apoptosis [4].

In conclusion, Cav3 channels, especially Cav3.2, are essential for various physiological functions, with a significant impact on pain, itch, NAFLD, and cerebral ischemia/reperfusion injury. Gene knockout mouse models have been instrumental in revealing their roles in these disease conditions, providing potential therapeutic targets for treatment.