Loss of physiological and structural functions of neurons induces neurodegenerative diseases, resulting in apoptosis and neuronal cell death. Neurodegenerative diseases include Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease.
One of the symptoms of these disorders may be the loss of coordination among the neurons and it ultimately progresses to marked degeneration of the peripheral and brain nerves. Intracellular free Ca2+ ([Ca2+]i) homeostasis is involved in many functions such as cellular viability, apoptosis, inflammation, physiological signal transduction, excessive microglia activation and overproduction of reactive oxygen species (ROS). Abnormal Ca2+ channel physiology and excessive level of oxidative stress have been implicated in a number of neurodegenerative diseases. The [Ca2+]i concentration is controlled by several membrane cation channels.
Transient receptor potential (TRP) channels are a family of non-selective cation channels that have important functions in the neurons. Their activations are very different from those of 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 channels is melastatin 2 (TRPM2), which is activated by ADP-ribose (ADPR). Nonetheless, TRPM2 and TRPV1 channels are activated and potentiated by oxidative stress. TRP Ankyrin 1 (TRPA1) is also an oxidative stress-sensitive Ca2+-permeable channel.
Despite the numerous basic and clinical research made on neuronal injury induced by neurodegenerative diseases, the involvement of TRP channels still remains elusive. In this Research Topic, we welcome submissions on oxidative stress dependent activated TRP channels such as TRPA1, TRPM2 and TRPV1 channels as novel targets for treating neurodegenerative diseases. With this collection we will add great support for the future direction of the novel targets in the management of neurodegenerative diseases.
Loss of physiological and structural functions of neurons induces neurodegenerative diseases, resulting in apoptosis and neuronal cell death. Neurodegenerative diseases include Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease.
One of the symptoms of these disorders may be the loss of coordination among the neurons and it ultimately progresses to marked degeneration of the peripheral and brain nerves. Intracellular free Ca2+ ([Ca2+]i) homeostasis is involved in many functions such as cellular viability, apoptosis, inflammation, physiological signal transduction, excessive microglia activation and overproduction of reactive oxygen species (ROS). Abnormal Ca2+ channel physiology and excessive level of oxidative stress have been implicated in a number of neurodegenerative diseases. The [Ca2+]i concentration is controlled by several membrane cation channels.
Transient receptor potential (TRP) channels are a family of non-selective cation channels that have important functions in the neurons. Their activations are very different from those of 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 channels is melastatin 2 (TRPM2), which is activated by ADP-ribose (ADPR). Nonetheless, TRPM2 and TRPV1 channels are activated and potentiated by oxidative stress. TRP Ankyrin 1 (TRPA1) is also an oxidative stress-sensitive Ca2+-permeable channel.
Despite the numerous basic and clinical research made on neuronal injury induced by neurodegenerative diseases, the involvement of TRP channels still remains elusive. In this Research Topic, we welcome submissions on oxidative stress dependent activated TRP channels such as TRPA1, TRPM2 and TRPV1 channels as novel targets for treating neurodegenerative diseases. With this collection we will add great support for the future direction of the novel targets in the management of neurodegenerative diseases.
