Transient receptor potential vanilloid (TRPV) channels: Basal properties and physiological potential

TRPV Channels in Osteoarthritis: A Comprehensive Review

“…In recent years, a growing number of studies have shown that TRP channels play anti-inflammatory and analgesic roles in joints while participating in the maintenance of their normal physiological functions [ 73 , 74 , 75 , 76 , 77 , 78 ]. For example, transient receptor potential vanilloid-1 (TRPV1) has been found to be an important transducer of chemical, inflammatory, and neuropathic pain signals, and is expressed in a variety of neuronal and non-neuronal tissues and organs, including chondrocytes, fibroblasts, macrophages, and the dorsal root ganglion (DRG), which play an important role in inflammatory diseases such as OA and rheumatoid arthritis [ 73 , 74 ].…”

“…For example, transient receptor potential vanilloid-1 (TRPV1) has been found to be an important transducer of chemical, inflammatory, and neuropathic pain signals, and is expressed in a variety of neuronal and non-neuronal tissues and organs, including chondrocytes, fibroblasts, macrophages, and the dorsal root ganglion (DRG), which play an important role in inflammatory diseases such as OA and rheumatoid arthritis [ 73 , 74 ]. Transient receptor potential vanilloid-4 (TRPV4) has been shown to respond directly or indirectly to a variety of mechanical signals, such as stretch, compression, osmotic pressure, and shear stress [ 75 ]. Recently, functional changes in TRPV1 and TRPV4 channels have been identified as risk factors for OA, and their abnormal expression and function can cause cell necrosis and apoptosis, cartilage extracellular matrix degradation, synovial inflammatory response, and hyperalgesia [ 76 , 77 , 78 ], suggesting that TRPV1 and TRPV4 play an important role in OA pain generation as well as disease progression.…”

Calcium and Neural Stem Cell Proliferation

“…Mechanical stimulation, pH, and osmotic pressure changes are among the stimuli involved in its activation. The physiological functions of these channels vary depending on the TRPV subtype and the tissue in which they are expressed [178] (Figure 4). To our knowledge, TRPV1, TRPV5, and TRPV6 do not participate in NSC proliferation or CNS development, while TRPV2, TRPV3, and TRVP4 participate in these processes.…”

TRPV3 Ion Channel: From Gene to Pharmacology

“…At the genetic level, potentially pathogenic variants of TRPV3 genes were identified in patients with small fiber neuropathy [120], migraine [121], and erythromelalgia [122]. Sensory hypoinnervation of the epidermis and, as a result, a deficit in sensations of acute mechanical pain, cold, and itching is observed in gain-of-function mutations of TRPV3, e.g., G573S [5]. In a behavioral pain model, mice with a mutant hyperactive TRPV3 (G573S) channel showed an increased mechanical threshold for pinpoint mechanical pain and a reduced response to acute pain compared to control littermates [123].…”

“…The TRP channel superfamily consists of seven subfamilies based on sequence homology: TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), TRPA (ankyrin), and TRPN (no mechanoreceptor potential C-like, or NOMPC-like) [1,2]. The TRPV subfamily includes TRPV1-TRPV6 members, which are widely expressed in both non-sensory and sensory cells, have high sequence similarity in different species, and display specific activation mechanisms and physiological functions (latest reviews [3][4][5]).…”