Abstract
Chronic pain syndromes are an important medical problem generated by various molecular, genetic, and pathophysiologic mechanisms. Back pain, neuropathic pain, and posttraumatic pain are the most important pathological processes associated with chronic pain in adults. Standard approaches to the treatment of them do not solve the problem of pain chronicity. This is the reason for the search for new personalized strategies for the prevention and treatment of chronic pain. The nitric oxide (NO) system can play one of the key roles in the development of peripheral pain and its chronicity. The purpose of the study is to review publications devoted to changes in the NO system in patients with peripheral chronical pain syndromes. We have carried out a search for the articles published in e-Library, PubMed, Oxford Press, Clinical Case, Springer, Elsevier, and Google Scholar databases. The search was carried out using keywords and their combinations. The role of NO and NO synthases (NOS) isoforms in peripheral pain development and chronicity was demonstrated primarily from animal models to humans. The most studied is the neuronal NOS (nNOS). The role of inducible NOS (iNOS) and endothelial NOS (eNOS) is still under investigation. Associative genetic studies have shown that single nucleotide variants (SNVs) of NOS1, NOS2, and NOS3 genes encoding nNOS, iNOS, and eNOS may be associated with acute and chronic peripheral pain. Prospects for the use of NOS inhibitors to modulate the effect of drugs used to treat peripheral pain syndrome are discussed. Associative genetic studies of SNVs NOS1, NOS2, and NOS3 genes are important for understanding genetic predictors of peripheral pain chronicity and development of new personalized pharmacotherapy strategies.
Highlights
Chronic pain syndromes are an important medical problem generated by various molecular, genetic, and pathophysiologic mechanisms
Recent studies have shown that NO synthases (NOS) enzymes play an important role in the development and chronicity of neuropathic, inflammatory, and post-traumatic pain
It is believed that afferent neurons in the spinal cord release glutamate to activate NMDA receptors, causing Ca2+ influx and NOS activation in neuropathic pain
Summary
Chronic pain syndromes are an important medical problem generated by various molecular, genetic, and pathophysiologic mechanisms. Neuropathic pain, and Chronic pain syndromes are an important medical problem generated by various molecular, genetic, and pathophysiologic mechanisms. Standard approaches to the treatment of these chronic pain synd2roof m18 es do not solve the problem of pain chronicity. This is the reason for the search for new personalized strategies for the prevention and treatment of chronic pain. Oted to changes in the NO system in patients with peripheral chronic pain syndromes. Oxidative stress may initiate or participate in matrix destruction and cell apoptosis, which result in disk degeneration [15]. Liu G.Z. et al (2001) and Rannou F. et al (2003) demonstrated that NO mediates the change of proteoglycan synthesis in the annulus fibrosus cells of the human intervertebral disc [17,18]
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