| Literature DB >> 32902792 |
Simin Tang1,2, Huan Jing1,3, Fuhu Song4, Haicheng Huang4, Wenjun Li4, Guiling Xie4, Jun Zhou5.
Abstract
Neuropathic pain (NP) can occur after peripheral nerve injury (PNI), and it can be converted into a maladaptive, detrimental phenotype that causes a long-term state of pain hypersensitivity. In the last decade, the discovery that dysfunctional microglia evoke pain, called "microgliopathic pain," has challenged traditional neuronal views of "pain" and has been extensively explored. Recent studies have shown that microRNAs (miRNAs) can act as activators or inhibitors of spinal microglia in NP conditions. We first briefly review spinal microglial activation in NP. We then comprehensively describe miRNA expression changes and their potential mechanisms in the response of microglia to nerve injury. We summarize the roles of the following two representative miRNAs: miR-124, which reverses NP by keeping microglia quiescent, and miR-155, which promotes NP following microglial activation. Finally, we focused on the therapeutic potential of microglial miRNAs in NP. The findings we summarized may be essential tools for basic research and clinical treatment of NP.Entities:
Keywords: MicroRNA; Microglia; Neuropathic pain; Peripheral nerve injury
Mesh:
Substances:
Year: 2020 PMID: 32902792 DOI: 10.1007/s12035-020-02102-1
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590