Molecular Pain最新文献

{"title":"EXPRESS: Preoperative reactive oxygen species exacerbate postoperative hyperalgesia by aggravating neuroinflammation through galectin-3.","authors":"Xuemei Zheng, Bin Shu, Ai Yan, Yonggang Liang, Niannian Huang, Houping Wang, Weilong Hong, Yongqin Chen, He Huang, Guangyou Duan","doi":"10.1177/17448069251353026","DOIUrl":"https://doi.org/10.1177/17448069251353026","url":null,"abstract":"<p><p>Patients with preoperative pathological conditions such as anxiety, depression, and sleep disorders experience more severe postoperative pain, suggesting that preoperative pathological changes in patients may affect postoperative pain. However, the potential pathophysiological changes associated with postoperative pain remain unknown. Here, this study initially employed clinical research to investigate potential pathophysiological changes related to postoperative pain. Subsequently, animal behavioral experiments and mechanistic explorations were conducted accordingly. Pregnant women undergoing cesarean sections who could provide preoperative cerebrospinal fluid were selected as subjects. Preoperative cerebrospinal fluid proteomics, postoperative pain intensity, and neutrophil-to-lymphocyte ratio (NLR) were analyzed. Rats were used to model the corresponding preoperative pathological state. Mechanical pain thresholds were measured after plantar incision and spinal cords were harvested for analysis. Clinical studies showed that one-quarter of the proteins positively correlated with postoperative pain were related to reactive oxygen species (ROS). Furthermore, the NLR-Ratio, reflecting postoperative inflammation level, increased with the severity of postoperative pain. Establishing a preoperative ROS-increased model with oxidant t-BOOH enhanced postoperative acute mechanical hyperalgesia and spinal neuroinflammation in rats. Conversely, preoperative administration of antioxidant VE, reducing ROS, alleviated postoperative hyperalgesia and spinal neuroinflammation. galectin-3 inhibitors mitigated postoperative hyperalgesia and neuroinflammation in the preoperative ROS-increased model. Additionally, The effects of galectin-3 on pain sensitization and pro-inflammation in vitro were mediated by the TLR4 receptor. Thus, this study demonstrated that preoperative ROS exacerbated postoperative hyperalgesia via galectin-3-mediated neuroinflammation, suggesting that galectin-3 may be a potential therapeutic target for alleviating postoperative pain in clinical patients.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251353026"},"PeriodicalIF":2.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESS: Circadian genes NPAS2 alleviate thermal nociceptive sensitization on CFA-induced inflammatory pain in mice.","authors":"Jiaqi Dong, Jingyi Wei, Hongwei Tong, Xiaohua Shi, Menghui Yuan, Yiwei Cao, Mohammed A El-Magd, Qiang Chen, Hongxin Zhang, Peng Yuan, Jiao Mu","doi":"10.1177/17448069251351045","DOIUrl":"https://doi.org/10.1177/17448069251351045","url":null,"abstract":"<p><p>Pain, particularly chronic pain, is a primary driver for patients seeking physical therapy. Inflammation is critically involved in both the pathogenesis and persistence of chronic pain. Neuronal PAS domain protein 2 (NPAS2), a core circadian transcriptional regulator, has been implicated in modulating pain-related stress responses. First, we investigated the expression of NPAS2 in nociceptive sensitized mice treated with CFA. Next, we systematically explored the effects of CFA on astrocyte and inflammatory factor release in NPAS2 knockout mice. The results showed that knockout of the NPAS2 gene did not affect the pain threshold of mice under normal physiological conditions, but reduced the mechanical and heat pain thresholds of 50% of CFA pedal-injected mice, resulting in nociceptive sensitization. It may be induced by promoting astrocyte activation and inducing cytokine (IL-1β, IL-6, TNF-α, NF-κB) expression. These findings suggest that NPAS2 could serve as both a prognostic biomarker for pain chronification and a novel therapeutic target for biologically tailored interventions.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251351045"},"PeriodicalIF":2.8,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESS: \"One coin, two aspects\": The role of IGF1R singling in chronic pain.","authors":"Yang Li, Shiyu Sun, Tong Liu, Guokun Zhou","doi":"10.1177/17448069251350856","DOIUrl":"https://doi.org/10.1177/17448069251350856","url":null,"abstract":"<p><p>Chronic pain, encompasses neuropathic and inflammatory pain, is a major public health burden. The insulin-like growth factor 1 receptor (IGF1R) has emerged as a critical player in pain modulation, exhibiting dual roles in both pain promotion and resolution. Recent studies have identified Follistatin (FST) as a novel ligand for IGF1R in neuropathic pain, where it activates the ERK/AKT signaling pathway, enhances Nav1.7-mediated sodium channel function, and induces neuronal hyperexcitability. Targeting the FST-IGF1R interaction with antagonist peptides has shown promise in alleviating neuropathic pain, highlighting its therapeutic potential. Conversely, IGF1/IGF1R signaling has also been implicated in pain resolution, particularly through CD11c+ microglia in the spinal dorsal horn, which promote recovery from neuropathic pain by phagocytosing myelin debris and modulating inflammatory responses. These findings underscore the context-dependent nature of IGF1R signaling, which can drive both nociceptive hypersensitivity and pain relief. This work synthesizes recent advances in understanding the multifaceted roles of IGF1R in chronic pain, offering novel insights into its mechanisms and therapeutic applications, and paving the way for the development of targeted therapies to address the complex challenges of chronic pain management.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251350856"},"PeriodicalIF":2.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESS: Administration of 2-deoxy-D-glucose alleviates cancer-induced bone pain by suppressing microglial polarization to the M1 phenotype and neuroinflammation.","authors":"Lin Liu, Dan-Yang Li, Long-Qing Zhang, Shao-Jie Gao, Fan-He Song, Jia-Yi Wu, Ya-Qun Zhou, Dai-Qiang Liu, Wei Mei","doi":"10.1177/17448069251348778","DOIUrl":"https://doi.org/10.1177/17448069251348778","url":null,"abstract":"<p><strong>Background: </strong>Cancer-induced bone pain (CIBP) is a debilitating complication with few effective treatments. Microglial activation contributes to the progression of CIBP. 2-deoxy-D-glucose (2-DG), a glycolytic inhibitor, could inhibit microglial activation. Its effect on CIBP remains unclear. This study aims to investigate the role of 2-DG in CIBP mice and underlying mechanisms.</p><p><strong>Methods: </strong>In this research, we established a CIBP mouse model by injecting Lewis lung cancer (LLC) cells into the bone marrow of the femur. Relevant pain behaviors were assessed by measuring the paw withdrawal threshold and spontaneous hind limb lifting. Additionally, the glycolysis inhibitor 2-DG was intrathecally administered to treat CIBP in mice. Western blotting and immunofluorescence techniques were employed to analyze microglial activation and M1/M2 phenotype markers in the spinal cord.</p><p><strong>Results: </strong>Our findings demonstrated significant microglial activation and polarization toward the M1 phenotype in the spinal cord of CIBP mice. Intrathecal administration of 2-DG effectively alleviated pain-related behaviors in CIBP mice. Furthermore, this treatment suppressed microglial activation and M1 polarization, while significantly restoring levels of the M2 phenotype. Additionally, 2-DG attenuated the production of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), while boosting the secretion of the anti-inflammatory factor (IL-10) in the spinal cord of CIBP mice. Notably, 2-DG effectively suppresses microglia activation and M1 polarization in LPS+IFN-γ-induced BV-2 cells by downregulating CD86, iNOS expression, TNF-α, IL-1β, IL-6 levels while upregulating Arg-1, CD206 expression and IL-10 level.</p><p><strong>Conclusion: </strong>These results suggest that 2-DG ameliorates mechanical allodynia, spontaneous pain and neuroinflammation in the spinal cord of CIBP mice by promoting the transition from the M1 phenotype to the M2 phenotype. This study may provide a novel strategy for the treatment of CIBP.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251348778"},"PeriodicalIF":2.8,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESS: Nanoparticulate MgH₂ Suppresses TRPM2-Mediated NLRP3 Inflammasome to Relieve Bone Cancer Pain.","authors":"Hang Xu, Hong-Tao Lu, Lu Lu, Zheng-Hao Li, Zhi-Sheng Piao, Yi Jia, Xiao-Yan Meng, Fei Xiang Wu","doi":"10.1177/17448069251348770","DOIUrl":"https://doi.org/10.1177/17448069251348770","url":null,"abstract":"<p><strong>Background: </strong>Bone cancer metastases are the third most common site of cancer spread after lungs and liver. This condition often causes severe pain that impairs patients' physical, psychological, and social well-being. We aimed to explore the potential therapeutic benefits of magnesium hydride (MgH2) on bone cancer pain (BCP).</p><p><strong>Methods: </strong>A BCP model was established in Wistar rats. Daily oral dosing of 0.5% w/w MgH2 was administered. Assessment included pain sensitivity, motor coordination, and emotional behaviors. Hippocampal samples underwent RNA sequencing, Western blotting, immunofluorescence, and quantitative RT-PCR.</p><p><strong>Results: </strong>MgH2 markedly reduced mechanical hypersensitivity and depressive behaviors in rats with BCP. These effects were linked to suppression of the TRPM2-NLRP3 signaling axis in hippocampal microglia. Additionally, MgH2 served as an adjuvant to reduce opioid tolerance during fentanyl co-treatment, enabling lower opioid dosages. Collectively, MgH2 inhibited TRPM2 activation, microglial activation, oxidative stress, and NLRP3 inflammasome formation, which together reduced neuroinflammation and improved therapeutic outcomes.</p><p><strong>Conclusion: </strong>MgH2 nanoparticles may relieve BCP and comorbid depressive symptoms by inhibiting TRPM2-mediated NLRP3 inflammasome activation in hippocampal microglia.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251348770"},"PeriodicalIF":2.8,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESS: TLR3 mediates central sensitization in a chronic migraine model induced by repeated nitroglycerin through the ERK signaling pathway.","authors":"Bin Yang, ZhaoMing Ge","doi":"10.1177/17448069251346373","DOIUrl":"https://doi.org/10.1177/17448069251346373","url":null,"abstract":"<p><strong>Background: </strong>Studies have demonstrated that Toll-like receptor 3 (TLR3) plays a crucial role in neuropathic pain. However, there have been no relevant reports regarding the role of TLR3 in mi-graine chronification. this study aims to investigate the molecular mechanisms of TLR3 in the cen-tral sensitization of chronic migraine (CM).</p><p><strong>Methods: </strong>C57BL/6 male mice were used as models for chronic migraine (CM) disease, receiving an intraperitoneal injection of nitroglycerin (NTG) every other day. Calibrated von Frey filaments were employed to measure the pain threshold in the hind paw sole and periorbital region, enabling the assessment of mechanical allodynia. Western blot was employed to detect the expression changes of TLR3, TRAF6, TAK1, c-Fos, calcitonin gene-related peptide (CGRP), and the extracellular signal-regulated kinase (ERK) signaling pathway. Immuno-fluorescence was used to detect the cellular localization of TLR3 and the expression changes of central sensitization-related indicators, such as c-Fos and CGRP. In addition, we investigated the effects of TLR3 inhibitor(CU CPT4a), MEK inhibitor(PD98059), TRAF6 inhibitor(C25-140), and TAK1 inhibitor (Takinib) on chronic migraine-like behavior, and activation of the ERK pathway in the Trigeminal nucleus caudalis(TNC).</p><p><strong>Results: </strong>Recurrent injections of NTG resulted in a signifi-cant increase in the expression of TLR3, TRAF6, TAK1, CGRP, and c-Fos proteins, as well as the activation of the ERK signaling pathway. Concurrent inhibition of TLR3 function, TRAF6, TAK1, and the ERK pathway counteracted these changes and alleviated hyperalgesia in CM mice. Con-clusions: Our findings suggest that TLR3 may play a role in central sensitization in CM mice by TRAF6-TAK1 axis modulating the ERK signaling pathway.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251346373"},"PeriodicalIF":2.8,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESS: Expression of Tacr1 and Gpr83 by spinal projection neurons.","authors":"Wenhui Ma, Allen Dickie, Erika Polgár, Mansi Yadav, Raphaelle Quillet, Maria Gutierrez-Mecinas, Andrew M Bell, Andrew Todd","doi":"10.1177/17448069251342409","DOIUrl":"https://doi.org/10.1177/17448069251342409","url":null,"abstract":"<p><p>Anterolateral system (ALS) projection neurons underlie perception of pain, itch and skin temperature. These cells are heterogeneous, and there have therefore been many attempts to define functional populations. A recent study identified two classes of ALS neuron in mouse superficial dorsal horn (SDH) based on expression of the G protein-coupled receptors Tacr1 or Gpr83. It was reported that cells expressing these receptors formed largely non-overlapping populations, and that ~60% of ALS cells in SDH expressed Tacr1. An additional finding was that while Tacr1- and Gpr83-expressing ALS cells projected to several brain nuclei, their axons did not reach the ventral posterolateral (VPL) thalamic nucleus, which is reciprocally connected to the primary somatosensory cortex. These results were surprising, because we had reported that ~90% of SDH ALS neurons in the mouse possess the neurokinin 1 receptor (NK1r), which is encoded by Tacr1, and in addition the VPL is thought to receive input from lamina I ALS cells. Here we use retrograde and anterograde labelling in Tacr1CreERT2 and Gpr83CreERT2 mice to reinvestigate the expression of the receptors by ALS neurons and to reassess their projection patterns. We find that ~90% of ALS neurons in SDH express Tacr1, with 40-50% expressing Gpr83. We also show that axons of both Tacr1- and Gpr83-expressing ALS neurons reach the VPL. These results suggest that ALS neurons in the SDH that express these GPCRs show considerable overlap, and that they are likely to contribute to the sensory-discriminative dimension of pain through their projections to VPL.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251342409"},"PeriodicalIF":2.8,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of excitatory synaptic transmission in the retrosplenial cortex of adult mice.","authors":"Jinjin Wan, Yujie Ma, Xuanying Chen, Wucheng Tao, Shun Hao, Wujun Geng, Yili Wu, Min Zhuo","doi":"10.1177/17448069251335500","DOIUrl":"https://doi.org/10.1177/17448069251335500","url":null,"abstract":"<p><p>The retrosplenial cortex (RSC) plays an important role in navigation, memory and pain. However, there are few studies on excitatory synaptic transmission in the RSC. Here, we used a multi-electrode array recording system (MED64) to study the characteristics of excitatory synaptic transmission in the RSC and the contribution of different types of voltage-gated Ca2+ channels (VGCCs) in excitatory synaptic transmission. We found that glutamate is the major excitatory transmitter for RSC, and postsynaptic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors contribute to excitatory synaptic transmission. We also found that the N-type calcium channel blocker ω-conotoxin GVIA (ω-Ctx GVIA) had a inhibitory effect on basal synaptic transmission. The inhibitory effect was not consistent across channels, suggesting that these excitatory synapses are not homogeneous for the contribution of presynaptic N-type VGCCs. Our findings provide strong evidence that excitatory synaptic transmission in the RSC is mainly mediated by AMPA receptors and that N-type VGCCs mediate fast synaptic transmission in the RSC of adult mice.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251335500"},"PeriodicalIF":2.8,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PDCD4 inhibition alleviates neuropathic pain by regulating spinal autophagy and neuroinflammation.","authors":"Ting Zhang, Le Qi, Kai Sun, Xiang Huan, Hao Zhang, Liwei Wang","doi":"10.1177/17448069251333928","DOIUrl":"10.1177/17448069251333928","url":null,"abstract":"<p><p>Neuropathic pain is still a clinical challenge. Inflammatory responses and autophagy in the spinal cord are important mechanisms for the occurrence and maintain of neuropathic pain. PDCD4 is an important molecule that regulates inflammation and autophagy. However, the regulatory role of PDCD4 is unknown in pain modulation. In this study we found that the expression of PDCD4 in the spinal cord of CCI mice was increased. Inhibition of PDCD4 by intrathecal injection of adeno-associated virus alleviated neuropathic pain hypersensitivity and enhanced autophagy in CCI mice, and inhibited the activation of MAPKs, as well as the expression of inflammatory factors. Intrathecal injection of autophagy inhibitor 3-MA reversed PDCD4 inhibition induced pain relief and change of autophagy. Our results indicate that spinal cord inhibition of PDCD4 alleviates pain sensitization in neuropathic pain mice through MAPKs and autophagy, and PDCD4 may be developed into a therapeutic target of neuropathic pain treatment.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251333928"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12056330/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143743090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced cancer perineural invasion induces profound peripheral neuronal plasticity, pain, and somatosensory mechanical deactivation, unmitigated by the lack of TNFR1. Part 2. Biophysics and gene expression.","authors":"Silvia Gutierrez, Renee A Parker, Morgan Zhang, Maria Daniela Santi, Yi Ye, Mario Danilo Boada","doi":"10.1177/17448069251323666","DOIUrl":"10.1177/17448069251323666","url":null,"abstract":"<p><p>Preclinical studies addressing the peripheral effects of cancer perineural invasion report severe neuronal availability and excitability changes. Oral cell squamous cell carcinoma perineural invasion (MOC2-PNI) shows similar effects, modulating the afferent's sensibility (tactile desensitization with concurrent nociceptive sensitization) and demyelination without inducing spontaneous activity (see Part 1.). The current study addresses the electrical status (normal or abnormal) of both active (low threshold mechano receptors (LT) and high threshold mechano receptors (HT)) and inactive (F-type and S-type) afferents. Concurrently, we have also evaluated changes in the genetic landscape that may help to understand the physiological dynamics behind MOC2-PNI-induced functional disruption of the peripheral sensory system. We have observed that the altered cell distribution and mechanical sensibility of the animal's somatosensory system cannot be explained by cellular electrical dysfunction or MOC2-PNI-induced apoptosis. Although PNI does modify the expression of several genes related to cellular hypersensitivity, these changes are insufficient to explain the MOC2-PNI-induced aberrant neuronal excitability state. Our results indicate that genetic markers provide limited information about the functional hyperexcitable state of the peripheral system. Importantly, our results also highlight the emerging role of plasma membrane Ca²⁺-ATPase activity (PMCA) in explaining several aspects of the observed gender-specific neuronal plasticity and the reported cellular distribution switch generated by MOC2-PNI.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251323666"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}