VAMP7, also known as vesicle-associated membrane protein 7, is a member of the SNARE proteins family. It plays a crucial role in intracellular vesicle transport, and is involved in pathways such as autophagy, unconventional secretion, and neurite growth [2,3,4]. In autophagy, it is part of the STX17-SNAP47-VAMP7/VAMP8 SNARE complex that mediates autophagosome-lysosome fusion, which is essential for the degradation of cellular contents [1]. In unconventional secretion, it is involved in the import of cytoplasmic proteins in membrane carriers and their release [2].

In VAMP7 knockout (KO) neuronal cells, neurite growth is impaired, suggesting that VAMP7-dependent secretion of Reticulon 3 regulates neurite growth [4]. In mast cells, VAMP7 knockdown impairs CCL2 secretion, indicating a role in regulating the secretion of specific inflammatory mediators [5]. In basophil-specific VAMP7 knockout (Ba-V7KO) mice, chronic itch is impaired, and skin levels of certain mediators are reduced, showing that VAMP7 is essential for basophil-driven chronic itch and acute itch flare in atopic dermatitis [6]. In pancreatic β-cells from male mice, VAMP7-deficient cells show defective autophagosome formation, accumulation of dysfunctional mitochondria, and impairment of glucose-stimulated insulin secretion, demonstrating its role in maintaining mitochondrial quality in these cells [7].

In conclusion, VAMP7 is vital for multiple biological processes including vesicle-mediated transport, autophagy, and the regulation of immune-related and neuronal functions. Gene knockout models, especially in neurons, mast cells, basophils, and pancreatic β-cells, have revealed its significance in processes related to neurite growth, cytokine secretion, atopic dermatitis, and mitochondrial homeostasis respectively, providing insights into potential therapeutic targets for related diseases.