Pain signalling pathways: from cytokines to ion channels.
Pain is the major reason patients seek medical care. The treatment of pain, particularly chronic pain associated with cancer and damage to the nervous system, is at present inadequate. Lack of effective analgesics is partly due to the fact that pain signalling mechanisms are still not fully understood. Over the recent years, many channels, receptors, and regulatory proteins involved in pain pathways have bee identified, and novel pain signalling mechanisms and pathways at peripheral and spinal levels have been discovered. It is anticipated that increased understanding of the molecular mechanisms of pain would provide a hope for the future development of effective pain killers. This review examines the currently available information on the molecular aspects of pain signalling pathways, and discusses novel and promising therapeutic targets for the treatment of pain in humans.
Okuse
Kenji
K
Division of Cell and Molecular Biology, Faculty of Natural Sciences, Imperial College London, London SW7 2AZ, UK. k.okuse@imperial.ac.uk
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001920:Bradykinin / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000378:metabolism*; D008954:Models, Biological; D020932:Nerve Growth Factor / Q000378:metabolism; D010146:Pain / Q000378:metabolism*; D011453:Prostaglandins / Q000378:metabolism; D012701:Serotonin / Q000378:metabolism; D015398:Signal Transduction; D050052:TRPC Cation Channels / Q000378:metabolism
D016207:Cytokines; D007473:Ion Channels; D011453:Prostaglandins; D050052:TRPC Cation Channels; D012701:Serotonin; D018698:Glutamic Acid; D000255:Adenosine Triphosphate; D020932:Nerve Growth Factor; D051546:Cyclooxygenase 2; D001920:Bradykinin