Abstract
Chronic pain (CP) is a severe clinical entity with devastating physical and emotional consequences for patients, which can occur in a myriad of diseases. Often, conventional treatment approaches appear to be insufficient for its management. Moreover, considering the adverse effects of traditional analgesic treatments, specialized pro-resolving lipid mediators (SPMs) have emerged as a promising alternative for CP. These include various bioactive molecules such as resolvins, maresins, and protectins, derived from ω-3 polyunsaturated fatty acids (PUFAs); and lipoxins, produced from ω-6 PUFAs. Indeed, SPMs have been demonstrated to play a central role in the regulation and resolution of the inflammation associated with CP. Furthermore, these molecules can modulate neuroinflammation and thus inhibit central and peripheral sensitizations, as well as long-term potentiation, via immunomodulation and regulation of nociceptor activity and neuronal pathways. In this context, preclinical and clinical studies have evidenced that the use of SPMs is beneficial in CP-related disorders, including rheumatic diseases, migraine, neuropathies, and others. This review integrates current preclinical and clinical knowledge on the role of SPMs as a potential therapeutic tool for the management of patients with CP.
Highlights
Chronic pain (CP) is one of the most frequent and difficult-to-manage clinical entities in medical practice [1]
specialized pro-resolving lipid mediators (SPMs) are synthesized in an active metabolic process in the latter stages of inflammation, acting as a regulatory mechanism, decreasing pain caused after sensitization of nociceptors, and limiting local tissue damage caused by the inflammatory response [11]
After activation of intracellular phospholipases, these molecules can be used as the initial substrate in the SPMs synthesis pathways, yielding products in two families: Lipoxins (LX), derived from arachidonic acid (AA), and protectins (PD), maresins (MaR), and resolvins (Rv), derived from the ω-3 fatty acids [18] (Figure 1)
Summary
Chronic pain (CP) is one of the most frequent and difficult-to-manage clinical entities in medical practice [1]. Multiple disorders featuring CP are the leading causes of disability worldwide, corresponding to a significant public health issues [2,3,4]; as well as marked reductions in quality of life related to restrictions of mobility and daily activities, anxiety, and depression [5,6]. Current pharmacological options for the treatment of CP are imperfect, including significant efficacy and tolerability issues [7]. Inflammation as a pathophysiologic component of pain has long been recognized in neural phenomena such as peripheral sensitization (PS), central sensitization (CS), and long-term spinal potentiation (LTP) [11]
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