期刊
ANESTHESIOLOGY
卷 115, 期 1, 页码 189-204出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/ALN.0b013e31821b1ac5
关键词
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资金
- National Institutes of Health (Bethesda, Maryland) [NS23970, 5RO1 NS 16996]
- Department of Veterans Affairs, Veterans Health Administration, Rehabilitation Research and Development Service (Washington, D. C.) [O4380-I, A6707-R]
- Brain Research Trust (London, United Kingdom)
- Department of Health's Comprehensive Biomedical Research Centre at University College London Hospitals National Health Service Foundation Trust (London, United Kingdom)
- Medical Research Council (London, United Kingdom)
- Christopher and Dana Reeve Foundation (Short Hills, New Jersey) [LMC-2010]
- William Heiser Foundation (Wantagh, New York)
- Abbott (Abbott Park, Illinois)
- Adolor (Exton, Pennsylvania)
- Array Biopharma (Boulder, Colorado)
- Johnson and Johnson (New Brunswick, New Jersey)
- Pfizer (New York, New York)
- Plexxikon (Berkeley, California)
- Roche (South San Francisco, California)
- Medical Research Council [G0601943] Funding Source: researchfish
- MRC [G0601943] Funding Source: UKRI
Nerve growth factor (NGF) was originally discovered as a neurotrophic factor essential for the survival of sensory and sympathetic neurons during development. However, in the adult NGF has been found to play an important role in nociceptor sensitization after tissue injury. The authors outline mechanisms by which NGF activation of its cognate receptor, tropomyosin-related kinase A receptor, regulates a host of ion channels, receptors, and signaling molecules to enhance acute and chronic pain. The authors also document that peripherally restricted antagonism of NGF-tropomyosin-related kinase A receptor signaling is effective for controlling human pain while appearing to maintain normal nociceptor function. Understanding whether there are any unexpected adverse events and how humans may change their behavior and use of the injured/degenerating tissue after significant pain relief without sedation will be required to fully appreciate the patient populations that may benefit from these therapies targeting NGF.
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