2013
DOI: 10.4236/ojapo.2013.23003
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Editorial: Apoptosis is Critical to Pain Control

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Cited by 5 publications
(7 citation statements)
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“…The most abundant pain sensors are in the skin and are called the transient receptor potential cation channels (TRP) [ 22 ]. The TRP family contains many members, such as the vanilloid receptors (TRPV), the canonical receptors (TRPC), the ankyrin repeat receptors (TRPA), the polycystin recaptors (TRPP), the melastatin receptors (TRPM), and the mucolipin receptors (TRPML) [ 22 ].…”
Section: Definition and Mechanisms Of Pain—a Brief Reviewmentioning
confidence: 99%
“…The most abundant pain sensors are in the skin and are called the transient receptor potential cation channels (TRP) [ 22 ]. The TRP family contains many members, such as the vanilloid receptors (TRPV), the canonical receptors (TRPC), the ankyrin repeat receptors (TRPA), the polycystin recaptors (TRPP), the melastatin receptors (TRPM), and the mucolipin receptors (TRPML) [ 22 ].…”
Section: Definition and Mechanisms Of Pain—a Brief Reviewmentioning
confidence: 99%
“…Excessive calcium permeability can cause apoptosis of sensory terminals. This causes long term pain relief until nerve terminals can be regenerated [ 4 ]. TRPs are also involved in inflammation in the skin and other sites in the body [ 2 ].…”
Section: Introductionmentioning
confidence: 99%
“…Among these, 11 pathways were considered the vital mechanisms involved in all of these three diseases. Neuronal apoptosis is a significant contributor to the development of hyperalgesia and sensitization particularly in neuropathic pain [ 79 ], and it is related to apoptosis-associated proteins such as caspases [ 80 ]. CP is associated with chronic neuroinflammation, the local inflammation in the peripheral or central nervous system [ 81 ].…”
Section: Discussionmentioning
confidence: 99%
“…Persistent chronic inflammation also increases the development of neurodegenerative diseases [ 82 ]. As an essential mechanism leading to neurodegeneration, apoptosis is also implicated [ 79 ] in the pathogenesis of neuropsychiatric diseases, such as anxiety and depression [ 83 ]. Advanced glycation end products (AGEs) interact with the receptor for AGEs (RAGE), contributing to an inflammatory and oxidative response [ 84 ].…”
Section: Discussionmentioning
confidence: 99%