Trpc3, a member of the mammalian transient receptor potential (TRP) superfamily of ion channels, is a Ca2+-permeable non-selective cation channel. It is activated by various stimuli such as G-protein coupled receptors, mechanical distortion of the plasma membrane, and diacylglycerols (DAG). It participates in many physiological processes, including maintaining cellular homeostasis, and is involved in pathways related to calcium signaling. Its functions are tissue-specific, with implications in the cardiovascular system, brain, immunity, cancer, and tissue remodeling [2].

In stress-induced senescent fibroblasts, down-regulation of Trpc3 promotes cytosolic/mitochondrial Ca2+ oscillations, elevates mitochondrial Ca2+ load, mitochondrial oxygen consumption rate, and oxidative phosphorylation. Re-expression of Trpc3 in senescent cells diminishes mitochondrial Ca2+ load and promotes escape from OIS-induced senescence. Also, Trpc3 down-regulation in stromal cells leads to a pro-inflammatory and tumour-promoting secretome that encourages cancer epithelial cell proliferation and tumour growth in vivo [1]. In Trpc3-/-mice, there is defective insulin secretion and glucose intolerance, indicating its role in islet beta-cell insulin secretion [3].

In conclusion, Trpc3 plays essential roles in multiple biological processes. Model-based research, especially gene knockout mouse models, has revealed its significance in diseases such as cancer and diabetes. Understanding Trpc3 provides insights into the underlying mechanisms of these diseases and may offer potential therapeutic targets.