Abstract
Transient receptor potential vanilloid 1 (TRPV1) is an ion channel expressed in sensory neurons, immune cells, pancreatic islets, and vascular tissues. Initially recognized for its role in thermosensation and nociception, TRPV1 has emerged as a key regulator of immune modulation, β-cell physiology, vascular integrity, and neuroimmune signaling-processes central to the pathogenesis and progression of Type 1 Diabetes (T1D). Experimental evidence demonstrates that TRPV1 exerts opposing effects on β-cell physiology-enhancing insulin release during short-term activation, yet accelerating stress and cell loss under chronic stimulation. In the vascular and renal systems, TRPV1 contributes to hallmark T1D complications, including endothelial dysfunction, nephropathy, and impaired cardiovascular protection, while in the central nervous system it drives neuroinflammation, cognitive decline, and emotional dysregulation. TRPV1 sensitization also accelerates the onset and severity of diabetic neuropathy by amplifying pain and inflammatory signaling pathways. Genetic and epigenetic regulation further links TRPV1 to individual susceptibility and disease progression. Collectively, these findings position TRPV1 as both a disease-modifying factor and a determinant of T1D outcomes, underscoring its potential as a biomarker and therapeutic target in autoimmune diabetes.