TRPC3 is a calcium-permeable non-selective cation channel that forms receptor-activated heterotetrameric complexes 1. It functions as a controller of intracellular calcium homeostasis through both inhibitory and activating calcium-binding sites that couple calcium concentration to channel activity 2. TRPC3 is activated via phospholipase C signaling pathways and diacylglycerol, particularly when responding to G-protein coupled receptor and receptor tyrosine kinase stimulation 3. The channel regulates ER-mitochondria calcium transfer, with downregulation promoting mitochondrial calcium overload and cellular senescence 4. TRPC3 is broadly expressed in pancreatic acinar cells, ductal epithelium, and endocrine islet cells 5, as well as thyroid follicular cells and C-cells 6. Functionally, TRPC3 mediates mechanical pain hypersensitivity through enhanced nociceptor excitability and spinal synaptic transmission via bradykinin-induced BDNF secretion 7. In cardiac tissue, TRPC3 interacts with NADPH oxidase 2 under hypoxic stress to regulate cardiac remodeling 8. Pathologically, TRPC3 mutations associate with spinocerebellar ataxia 41, while TRPC3 dysfunction contributes to cellular senescence-associated pro-tumoral inflammation.