Molecular and Cellular Mechanisms of Pain
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: closed (20 August 2015) | Viewed by 53071
Special Issue Editor
Interests: nerve injury and neuropathic pain; pain and aging; central adaptations to chronic pain; multiple sclerosis; neuroinflammation; neuro-immunologic communication; redox signaling; nitric oxide; endocannabinoids and other lipid signaling molecules; progranulin; autophagy
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Growing numbers of molecules have been suggested to contribute to the development of chronic inflammatory or neuropathic pain. Based on rodent models, some of these molecules have potential as drug targets, such as fatty acid amide hydrolase, which regulates the metabolism of endocannabinoids, and GTP cyclohydrolase, which is the key enzyme in tetrahydrobiopterin synthesis. However, so far, no compounds have reached clinical practice and patients have few therapeutic options. No matter the reason for the pain, treatment focuses on symptom relief, but does not address or cure the underlying pathology of pain signaling. Available therapeutics either target opioid and cannabinoid receptors or cyclooxygenases or nonspecifically lower neuronal excitability. Pain relief via these drugs is associated with side effects. Therefore, there is still a high clinical need for novel pain-therapeutics that would address the underlying causes. Thus, there is a continuing search for targetable molecules and cellular processes, such as neuronal death. Also, there is continuing research concerning the interplay of neurons, glial cells, and immune cells. One approach is the targeting of activated (micro)glia for treatment of neuropathic pain because these cells produce pro-inflammatory substances, which maintain hyperexcitability in nociceptive neurons, even if the nerve injury is healed. The glia activation is driven by, e.g., specific purine receptors, cytokines, and growth factors, and are inhibited by inflammation resolving lipid signaling molecules, which are all potentially interesting drug targets. Transient receptor potential channels and specific sodium channels are long known as key molecules for nociception and there are some intelligent drugs that enter through one channel and then target the other from inside (to confer some specificity). However, successful pain reduction in rodents only moderately predicts efficacy in humans, because the pain goes far beyond nociception and behavioral tests in rodents rely mostly on the stimulation of an inflamed or nerve injured paw, but do not measure spontaneous pain or long-term adaptive changes in pain-associated centers. Thus, pain-causing or pain-resolving molecules must be seen in a broader context of pain as a systemic disease.
Prof. Dr. Irmgard Tegeder
Guest Editor
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
Keywords
- microglia
- neuronal apoptosis
- purine receptors
- TRP channels
- cytokines
- hyperexcitability
- cannabinoids
- opioids
- lipid signaling molecules
Benefits of Publishing in a Special Issue
- Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
- Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
- Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
- External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
- e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.
Further information on MDPI's Special Issue polices can be found here.
