RT Journal Article
T1 Sigma-1 receptor: A drug target for the modulation of neuroimmune and neuroglial interactions during chronic pain.
A1 Ruiz-Cantero, M Carmen
A1 Gonzalez-Cano, Rafael
A1 Tejada, Miguel A
A1 Santos-Caballero, Miriam
A1 Perazzoli, Gloria
A1 Nieto, Francisco R
A1 Cobos, Enrique J
K1 Astrocyte
K1 Endogenous opioid analgesia
K1 Macrophage
K1 Microglia
K1 Neuroinflammation
K1 Pain
AB Immune and glial cells play a pivotal role in chronic pain. Therefore, it is possible that the pharmacological modulation of neurotransmission from an exclusively neuronal perspective may not be enough for adequate pain management, and the modulation of complex interactions between neurons and other cell types might be needed for successful pain relief. In this article, we review the current scientific evidence for the modulatory effects of sigma-1 receptors on communication between the immune and nervous systems during inflammation, as well as the influence of this receptor on peripheral and central neuroinflammation. Several experimental models of pathological pain are considered, including peripheral and central neuropathic pain, osteoarthritic, and cancer pain. Sigma-1 receptor inhibition prevents peripheral (macrophage infiltration into the dorsal root ganglion) and central (activation of microglia and astrocytes) neuroinflammation in several pain models, and enhances immune-driven peripheral opioid analgesia during painful inflammation, maximizing the analgesic potential of peripheral immune cells. Therefore, sigma-1 antagonists may constitute a new class of analgesics with an unprecedented mechanism of action and potential utility in several painful disorders.
PB Elsevier Ltd
YR 2020
FD 2020-11-23
LK http://hdl.handle.net/10668/16733
UL http://hdl.handle.net/10668/16733
LA en
NO Ruiz-Cantero MC, González-Cano R, Tejada MÁ, Santos-Caballero M, Perazzoli G, Nieto FR, et al. Sigma-1 receptor: A drug target for the modulation of neuroimmune and neuroglial interactions during chronic pain. Pharmacol Res. 2021 Jan;163:105339.
NO M.C. Ruiz-Cantero was supported by the Training University Lecturers program (FPU) of the Spanish Ministry of Economy and Competitiveness (MINECO). M.Á. Tejada was supported by a postdoctoral grant from the Biomedical Research Institute, Hospital Clínico Universitario in Valencia (INCLIVA). This study was partially supported by the Spanish State Research Agency (10.13039/501100011033) under the auspices of MINECO (grant numbers SAF2016-80540-R  and PID2019-108691RB-I00), the Andalusian Regional Government (grant CTS109), and the European Regional Development Fund. We thank K. Shashok for improving the use of English in the manuscript.
DS RISalud
RD Apr 12, 2025