The clinical management of chronic pain has long relied on traditional drugs such as opioids, anti-inflammatory drugs, and anticonvulsants, but generally faces issues of insufficient efficacy and significant side effects. There is an urgent need for novel therapeutic strategies targeting pain mechanisms. Recent studies have shown that T-type calcium channels play a key role in the development of neuropathic and inflammatory pain. Their expression and function are significantly upregulated in dorsal root ganglion and spinal dorsal horn neurons, making them a highly promising analgesic target. However, the development of direct Cav3.2 subtype channel blockers still faces challenges such as low subtype selectivity, and central nervous system and cardiovascular side effects. Currently, no ideal clinical candidate drug has emerged. This article systematically reviews the role of calcium signaling in chronic pain mechanisms, focusing on analyzing the pathological functions of T-type calcium channels (particularly the Cav3.2 subtype) and the research progress and translational challenges of their inhibitors. The aim is to provide a theoretical basis and directional guidance for developing efficient and safe pain treatment strategies.