ArticleCNS neuroscience & therapeutics2026
STING Modulating ER-Phagy in the Prelimbic Cortex Neurons Contributed to Neuropathic Pain and Emotional Comorbidity.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOur previous data suggested that autophagy is crucial for neuropathic pain. The different cell types and varying degrees of regulation of STING may lead to a paradoxical effect on pain and emotions in the neuropathic pain model. Up to now, whether STING modulates neuropathic pain in PrL neurons via ER-phagy is still unknown.
methodIn this study, we investigated the effect of ER-phagy in the prefrontal cortex (PrL) on neuropathic pain. We administered 4-phenylbutyric acid, tunicamycin, 3-methyladenine, and rapamycin to evaluate the interaction between endoplasmic reticulum (ER) stress and autophagy in the PrL of SNL (spinal nerve ligation). We injected AAV to investigate whether ER-phagy modulated pain and emotional behaviors. We further explored whether STING and its pathway as a modulation target for ER-phagy to participate in the pain process. We injected 2'3-cGAMP and RU521 to modulate the cGAS/STING pathway in ER-phagy in SNL mice. Moreover, we modulated STING expression and regulated the levels of ER-phagy and the interaction between STING and LC3 in neurons through PrL AAV injections.
resultsThe data indicated that ER-phagy alleviated the excessive ER stress induced by SNL in PrL through the cGAS/STING pathway. Regulating ER-phagy in PrL neurons through AAV tools altered pain and emotion-related behaviors. In addition, regulating STING in PrL neurons altered the comorbidity of pain and emotion. Importantly, the binding interaction between STING and LC3 in PrL neurons provides a novel target for PrL ER-phagy.
conclusionEnhanced ER-phagy of PrL neurons provides analgesic, anti-anxiety, and antidepressant effects through modulating STING in SNL mice.
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