Neuropathic pain has a tremendous impact on quality of life in diseases such as diabetes and cancer. One of the symptoms of this disorder might be pain and it ultimately progresses to marked degeneration of the peripheral nerves. Intracellular free Ca2+ ([Ca2+]i) homeostasis is involved in many functions such as cellular viability, apoptosis, physiological signal transduction and over production of reactive oxygen species (ROS). Abnormal Ca2+ channel physiology and excessive level of oxidative stress have been implicated in a number of pain states in the diseases. The [Ca2+]i concentration is controlled by a number of membrane cation channels. Transient receptor potential (TRP) channels are a family of non-selective cation channels that have important functions in DRG neurons. Their activations are very different from voltage gated calcium and chemical channels. In addition, some of TRP channels are activated by oxidative stress. For example, TRP vanilloid type 1 (TRPV1) channel is a polymodal receptor permeable to cations and activated by a pungent chemical from chili peppers (capsaicin), as well as by low pH and noxious heat. Another subfamily of TRP is melastatin 2 (TRPM2) channel and it is activated by ADP-ribose (ADPR). Nonetheless, TRPM2 and TRPV1 channels are activated and potentiated by oxidative stress. TRP Ankyrin 1 (TRPA1) is also oxidative stress-sensitive Ca2+-permeable channels. In recent studies we observed that the TRPA1, TRPM2 and TRPV1 play an important role in the pain transmission of sensory neurons, including the dorsal root ganglion (DRG). The expression levels of TRPA1, TRPM2 and TRPV1 are highest in the DRG. Diabetes causes neurotoxicity and peripheral neuropathies through excessive apoptosis, mitochondrial oxidative stress and overload Ca2+ entry. Peripheral neuropathies are also a common side effect of treatment of various chemotherapeutics (oxaliplatin, cisplatin, paclitaxel and the like). Despite numerous basic and clinical researchers made by the anticancer drug and disease (such as diabetes and mechanical injuries)-induced peripheral neuropathy study the mechanism is not well understood. In the specific research topic of the journal, we will welcome results of oxidative stress dependent activated TRP channels such as TRPA1, TRPM2 and TRPV1 channels as novel targets for treating peripheral pain. We will also welcome ‘pain and TRP channels’, ‘pain and oxidative stress’ and ‘pain, oxidative stress and pain’ manuscripts.
Neuropathic pain has a tremendous impact on quality of life in diseases such as diabetes and cancer. One of the symptoms of this disorder might be pain and it ultimately progresses to marked degeneration of the peripheral nerves. Intracellular free Ca2+ ([Ca2+]i) homeostasis is involved in many functions such as cellular viability, apoptosis, physiological signal transduction and over production of reactive oxygen species (ROS). Abnormal Ca2+ channel physiology and excessive level of oxidative stress have been implicated in a number of pain states in the diseases. The [Ca2+]i concentration is controlled by a number of membrane cation channels. Transient receptor potential (TRP) channels are a family of non-selective cation channels that have important functions in DRG neurons. Their activations are very different from voltage gated calcium and chemical channels. In addition, some of TRP channels are activated by oxidative stress. For example, TRP vanilloid type 1 (TRPV1) channel is a polymodal receptor permeable to cations and activated by a pungent chemical from chili peppers (capsaicin), as well as by low pH and noxious heat. Another subfamily of TRP is melastatin 2 (TRPM2) channel and it is activated by ADP-ribose (ADPR). Nonetheless, TRPM2 and TRPV1 channels are activated and potentiated by oxidative stress. TRP Ankyrin 1 (TRPA1) is also oxidative stress-sensitive Ca2+-permeable channels. In recent studies we observed that the TRPA1, TRPM2 and TRPV1 play an important role in the pain transmission of sensory neurons, including the dorsal root ganglion (DRG). The expression levels of TRPA1, TRPM2 and TRPV1 are highest in the DRG. Diabetes causes neurotoxicity and peripheral neuropathies through excessive apoptosis, mitochondrial oxidative stress and overload Ca2+ entry. Peripheral neuropathies are also a common side effect of treatment of various chemotherapeutics (oxaliplatin, cisplatin, paclitaxel and the like). Despite numerous basic and clinical researchers made by the anticancer drug and disease (such as diabetes and mechanical injuries)-induced peripheral neuropathy study the mechanism is not well understood. In the specific research topic of the journal, we will welcome results of oxidative stress dependent activated TRP channels such as TRPA1, TRPM2 and TRPV1 channels as novel targets for treating peripheral pain. We will also welcome ‘pain and TRP channels’, ‘pain and oxidative stress’ and ‘pain, oxidative stress and pain’ manuscripts.
