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Role of autophagy in the pathogenesis and regulation of pain

Pain is a ubiquitous and highly concerned clinical symptom, usually caused by peripheral or central nervous injury, tissue damage, or other diseases. The long-term existence of pain can seriously affect daily physical function and quality of life and produce great torture on the physiological and ps...

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Bibliographic Details
Published in:European journal of pharmacology 2023-09, Vol.955, p.175859-175859, Article 175859
Main Authors: Zheng, Guangda, Ren, Juanxia, Shang, Lu, Bao, Yanju
Format: Article
Language:English
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Summary:Pain is a ubiquitous and highly concerned clinical symptom, usually caused by peripheral or central nervous injury, tissue damage, or other diseases. The long-term existence of pain can seriously affect daily physical function and quality of life and produce great torture on the physiological and psychological levels. However, the complex pathogenesis of pain involving molecular mechanisms and signaling pathways has not been fully elucidated, and managing pain remains highly challenging. As a result, finding new targets to pursue effective and long-term pain treatment strategies is required and urgent. Autophagy is an intracellular degradation and recycling process that maintains tissue homeostasis and energy supply, which can be cytoprotective and is vital in maintaining neural plasticity and proper nervous system function. Much evidence has shown that autophagy dysregulation is linked to the emergence of neuropathic pain, such as postherpetic neuralgia and cancer-related pain. Autophagy has also been connected to pain caused by osteoarthritis and lumbar disc degeneration. It is worth noting that in recent years, studies on traditional Chinese medicine have also proved that several traditional Chinese medicine monomers involve autophagy in the mechanism of pain relief. Therefore, autophagy can serve as a potential regulatory target to provide new ideas and inspiration for pain management.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2023.175859