Trpv2, or Transient Receptor Potential Vanilloid type 2, is a calcium-permeable cation channel belonging to the TRPV channel family. It is activated by heat (>52 °C), various ligands, and mechanical stresses. Under unstimulated conditions, a large portion of it is located in the endoplasmic reticulum, and upon certain stimulations like phosphatidylinositol 3-kinase-activating ligands or mechanical stress, it translocates to the plasma membrane to function as a cation channel. It is highly expressed in neurons, neuroendocrine cells, immune cells involved in innate immunity, and certain cancer cells, modulating various cellular functions [1].

In B cells, TRPV2 is highly expressed and plays a crucial role in the formation of the B cell immunological synapse and B cell activation. Mice with deficient TRPV2 in B cells display impaired antibody responses following immunization, indicating its importance in B cell-mediated immune functions [2]. In the context of heart failure and muscular dystrophy-related cardiomyopathy, TRPV2 is a stretch-sensitive channel that causes sustained intracellular Ca2+ increase in muscular cells. Inactivation of TRPV2 in animal models of cardiomyopathy with heart failure ameliorates muscle dysgenesis, improves cardiac function, and survival prognosis [3,4]. Regarding viral infections, the interferon-stimulated gene TRIM21 interacts with and degrades TRPV2 in myeloid cells. Trim21-/-mice are more susceptible to HSV-1 and VSV infection, and this susceptibility is rescued by inhibition or deletion of TRPV2 [5].

In conclusion, Trpv2 is a key ion channel involved in multiple biological processes. Its role in B cell activation, heart failure, muscular dystrophy-related cardiomyopathy, and viral infections has been revealed through gene-knockout or conditional-knockout mouse models. Understanding Trpv2 function provides potential therapeutic targets for related diseases.