Special Issue "Emerging Pain Targets and Therapy"

Guest Editor
Dr. Kim Lawson
Department of Biosciences, Biomedical Research Centre, Sheffield Hallam University, Faculty of Health and Wellbeing, City Campus, Sheffield, S1 1WB, UK
E-Mail: k.lawson@shu.ac.uk
Interests: fibromyalgia; pain; potassium channels; drug design/discovery

Dear Colleagues,

Pain remains a major clinical challenge with the management of pain the most frequent issue encountered by clinicians. Many current analgesics are limited by serious unwanted effects, while for some pain conditions there are no effective analgesics. Advances in molecular biological techniques that have enabled the discovery of specific molecules involved in pain production have contributed to a better understanding of pain and the mechanisms of different types of pain and are providing clues for the development of novel pharmacotherapies for specific pain types. This increased understanding of pain physiology has offered a number of potential targets (e.g. TRPV1, voltage-gated sodium channels, calcium channels, glutamate receptors, cannabinoids) for future treatments, in particular for neuropathic and chronic pain. This special issue is intended to provide the reader with an insight into the progress made in this field through novel contributions of original papers and critical reviews.

Dr. Kim Lawson
Guest Editor

Submission

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• pain
• pain pathways
• emerging targets
• molecular biology
• novel therapies
• ion channels

Type of the Paper: Review
Title: Role of Transient Receptor Potential Vanilloid 1 in Inflammation and Autoimmune Diseases
Authors: Fumio Tsuji and Hiroyuki Aono
Affiliation: Research and Development Center, Santen Pharmaceutical Co.,Ltd., Japan; E-Mail: ftsuji@minuet.plala.or.jp
Abstract: The transient receptor potential vanilloid-1 (TRPV1) cationchannel is a receptor that is activated by noxious temperatures, as well as to chemical agonists, such as vanilloids and protons. With these properties, TRPV1 has emerged as a polymodal nocisensor of nociceptive afferent neurons. As many proalgesic pathways converge on TRPV1 and it is upregulated and sensitized by inflammation and injury, TRPV1 is thought to be a central transducer of hyperalgesia and a prime target for the pharmacological control of pain. However, there is conflicting evidence to date as to whether TRPV1 agonists promote or inhibit inflammation. We recently demonstrated that SA13353 [1-[2-(1-adamantyl)ethyl]-1-pentyl-3-[3-(4-pyridyl)propyl]urea], a novel TRPV1 agonist, inhibits tumor necrosis factor-? production through the activation of capsaicin-sensitive afferent neurons and reduces the severity of symptoms of kidney injury, lung inflammation, arthritis and encephalomyelitis in disease models. These results suggest that TRPV1 agonists may act in an anti-inflammatory manner in vivo in certain inflammatory and autoimmune diseases and conditions. The use of potent TRPV1 antagonists as a general strategy to treat inflammation must be cautiously considered, given the deleterious effects that may arise from inhibiting the population of channels that have a protective function. Further studies to clarify the role of TRPV1 in inflammation and autoimmune diseases are therefore necessary.