Molecular Pain最新文献

{"title":"Beyond restless sleep: A cross-sectional study of obstructive sleep apnea risk, aging biomarkers, and chronic low back pain.","authors":"Khalid W Freij, Fiona Bat Agbor, Philemon Domoyeri, Kiari R Kinnie, Asia M Wiggins, Demario S Overstreet, Tammie L Quinn, Shivraj S Grewal, S Justin Thomas, Walid W Freij, Shameka L Cody, Michael A Owens, Robert E Sorge, Burel R Goodin, Edwin N Aroke","doi":"10.1177/17448069261427979","DOIUrl":"10.1177/17448069261427979","url":null,"abstract":"<p><p>This secondary data analysis aimed to determine the nature of the relationship between obstructive sleep apnea (OSA) risk, biological age acceleration, and nonspecific chronic low back pain (CLBP). In total, 199 adults aged 18-82 years who filled both STOPBANG and pain questionnaires subsetted for secondary analysis. Based on the STOPBANG questionnaire, 104 had a low OSA risk and 95 had an intermediate or high OSA risk. Dunedin Pace of Aging Computed from the Epigenome (DunedinPACE), Horvath's, Hannum's, PhenoAge, and GrimAge clocks were used to determine biological age and pace of biological aging. Individuals with low OSA risk reported increased DunedinPACE compared to those with intermediate/high OSA risk (<i>p</i> < 0.001). There was a significant correlation between the risk for OSA and biological age acceleration measured by PhenoAge as well as pace of biological aging (<i>p</i> < 0.05). Mediation analysis detected indirect effects of OSA risk on chronic pain outcomes through the pace of biological aging. Targeted interventions addressing OSA risk offers a promising therapeutic strategy. This could be particularly valuable for aging populations where both accelerated biological aging and chronic pain conditions are prevalent, offering a more holistic approach to improving nonspecific chronic pain outcomes through quality of sleep and restfulness.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261427979"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146213443","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":"Contralateral electroacupuncture modulates the transmission of nociceptive information in the spinal dorsal horn via GABAergic neurons in the rostral ventromedial medulla.","authors":"Kailing Zhang, Qingquan Yu, Yang Yang, He Zhu, Lingling Yu, Zhiyun Zhang, Kexing Wan, Jiajia Huang, Ping Peng, Jiwei Yao, Xianghong Jing, Man Li","doi":"10.1177/17448069261421426","DOIUrl":"10.1177/17448069261421426","url":null,"abstract":"<p><p>Recent studies have shown that electroacupuncture (EA) can exert analgesic effects by modulating wide dynamic range (WDR) neurons in the spinal dorsal horn; however, how EA regulates WDR neurons to inhibit pain signals remains unclear. In this study, we identified a key brain region, rostral ventromedial medulla (RVM), involved in the modulation of spinal WDR neurons. Subsequently, we found evidence suggesting that GABAergic neurons in the RVM may mediate the transmission of nociceptive and non-nociceptive signals from the spinal cord, which underlies EA analgesia. The results demonstrated that the activation of RVM GABAergic neurons enhanced the excitability of WDR neurons, thereby facilitating the transmission of peripheral sensory signals within the spinal cord. Contralateral EA at 2 mA effectively suppressed WDR neuron activity and elevated pain thresholds in rats modeled with complete Freund's adjuvant (CFA). Notably, heightened activity of RVM GABAergic neurons mitigated the inhibitory effects of EA on WDR neurons and reduced EA-induced analgesia. These findings suggest that EA may attenuate WDR neuronal activity by modulating RVM GABAergic neurons, thereby inhibiting nociceptive transmission. This study highlights the potential involvement of RVM GABAergic neurons and identifies the efficacy of high-intensity, contralateral EA stimulation in producing analgesia.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261421426"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147276477","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":"miRNA-let7b5p alleviates visceral hypersensitivity by inhibiting the activation of spinal microglial in male IBS-like rats.","authors":"Xianhe Wu, Ying Tang, Zhengqing He, Fan Yang, Yiqian Liu, Qianli Zhang, Aiqin Chen, Yu Chen, Chun Lin","doi":"10.1177/17448069261430202","DOIUrl":"10.1177/17448069261430202","url":null,"abstract":"<p><p>Visceral hypersensitivity is a hallmark feature of irritable bowel syndrome (IBS), yet its underlying mechanisms remain incompletely understood. In the present study, we found that miRNA-let7b5p was downregulated in the spinal cord of IBS model rats induced by neonatal colorectal distension. Concurrently, microglia exhibited a shift toward a pro-inflammatory M1 phenotype and selectively engulfed inhibitory synapses, resulting in impaired GABAergic neuronal function and disruption of the excitatory/inhibitory balance. Intrathecal administration of a miRNA-let7b5p agomir suppressed M1-type microglial activation in the spinal cord, reduced pro-inflammatory cytokine levels, and alleviated visceral hypersensitivity, whereas antagomir treatment induced visceral hypersensitivity in control rats. Mechanistically, MAP3K3 was identified as a direct target of miRNA-let7b5p, and its knockdown recapitulated the protective effects conferred by miRNA upregulation. Collectively, these findings demonstrate that miRNA-let7b5p attenuates IBS-associated visceral hypersensitivity by downregulating MAP3K3, thereby inhibiting spinal microglial activation and restoring GABAergic neuronal function. This study provides novel insights into the pathogenesis of IBS-related visceral hypersensitivity and highlights a potential therapeutic target for drug development.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261430202"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355999","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":"Circulating cellular senescence biomarkers in persons with chronic knee osteoarthritis pain: An exploratory study.","authors":"Muhammad Abbas, Javier A Tamargo, Carlos J Cruz, Yutao Zhang, Stephanie Wohlgemuth, Kevin Wu, Li Chen, Roland Staud, Roger B Fillingim, Christiaan Leeuwenburgh, Yenisel Cruz-Almeida","doi":"10.1177/17448069261422994","DOIUrl":"10.1177/17448069261422994","url":null,"abstract":"<p><p>The senescence-associated secretory phenotype (SASP) contributes to tissue degeneration and inflammation, yet its role in osteoarthritis (OA)-related pain remains poorly understood. We hypothesized that circulating SASP markers would be associated with distinct OA-pain phenotypes, defined by pain impact and radiographic OA (ROA) severity. A subset of middle-to-older-aged adults (45-85 years) from a larger multi-site study (<i>n</i> = 169) self-reported pain impact - defined as the extent to which pain interferes with daily functioning - and underwent knee radiography and blood collection. Hierarchical cluster analysis was used to empirically identify OA-pain phenotypes based on combined pain impact and Kellgren-Lawrence (KL) grade. Plasma levels of four SASP markers (GDF-15, activin-A, Osteopontin (OPN), and IL-15) were quantified from whole blood samples. Among 169 participants, 35.5% reported high-impact chronic knee pain and 27.8% exhibited moderate-to-severe radiographic OA. Cluster analysis identified distinct ROA-pain phenotypes. GDF-15 levels were significantly elevated in non-Hispanic White females with early ROA and high-impact pain, with race- and sex-dependent differences. Activin-A levels were higher in non-Hispanic Black participants without pain or ROA and varied by sex in early ROA/low-impact pain phenotypes. Osteopontin levels were elevated in males compared to females within the same phenotype group. IL-15 levels showed no association with ROA-pain phenotypes but were higher in males and positively correlated with age. SASP factors, particularly GDF-15, Activin-A, and Osteopontin, demonstrated race- and sex-dependent associations with OA-pain phenotypes. These findings underscore the importance of demographic context in OA pathophysiology and support further investigation into SASP factors as potential biomarkers and therapeutic targets for OA-related pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261422994"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12929831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100512","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":"The enhanced analgesic effects of electroacupuncture and repetitive transcranial magnetic stimulation on visceral pain via ventral lateral septal nucleus.","authors":"Rui-Xia Weng, Yuan Gao, Chen-Hao Zhang, Ru-Yu Yan, Qi Liu, Zhen-Hua Xu, Hua-Zheng Wang, Rui Li, Rong Gao, Yong-Chang Li, Guang-Yin Xu","doi":"10.1177/17448069261428970","DOIUrl":"10.1177/17448069261428970","url":null,"abstract":"<p><p>Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder characterized primarily by chronic visceral pain, with a complex pathogenesis and limited efficacy of current therapeutic interventions. Growing evidence indicates that electroacupuncture (EA) and repetitive transcranial magnetic stimulation (rTMS) exert significant analgesic effects on visceral pain. However, the underlying neural circuit mechanisms remain poorly understood. In this study, the ventral part of the lateral septal nucleus (LSV) was identified as a critical brain region mediating the analgesic effects of EA and rTMS in a mouse model of visceral pain. Visceral nociceptive stimulation significantly increased c-Fos expression in the LSV, predominantly within glutamatergic (Glu⁺) neurons. Optogenetic inhibition of LSV Glu⁺ neurons attenuated visceral pain, whereas their activation exacerbated pain-related behaviors. Both EA and rTMS individually reduced visceral pain-induced c-Fos expression and alleviated pain behaviors, with the combined EA + rTMS treatment producing a more pronounced analgesic effect than either treatment alone. Moreover, fiber photometry recordings demonstrated that EA and rTMS decreased glutamate release and concurrently increased cannabinoid signaling in the LSV, suggesting that these interventions modulate neurotransmitter dynamics to regulate neuronal excitability. In summary, our findings highlight the pivotal role of LSV Glu⁺ neurons in the modulation of visceral pain. EA and rTMS exert their therapeutic effects by regulating glutamate and cannabinoid release within this circuit. These insights provide a foundation for developing targeted neuromodulatory strategies for the treatment of chronic visceral pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261428970"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13087329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513828","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":"CXCL12/CXCR4 axis in neuropathic pain: Insights from preclinical models and translational implications.","authors":"Ming Li, Xiao-Xiao Lu, Lu-Yao Cai, Tao Zhu, Jin Cui","doi":"10.1177/17448069261444493","DOIUrl":"10.1177/17448069261444493","url":null,"abstract":"<p><p>Neuropathic pain affects approximately 7%-10% of the global population, significantly impairing patients' quality of life and placing a substantial burden on public health systems. Current pharmacological treatments have limited efficacy and are often accompanied by notable side effects, highlighting the urgent need for novel therapeutic targets. Increasing evidence supports the important role of chemokines and their receptors in neuro-immune interactions underlying pain sensitization. Among these pathways, the CXCL12/CXCR4 axis has emerged as an important regulator of both the initiation and maintenance of neuropathic pain. Beyond its canonical function in immune cell trafficking, the CXCL12/CXCR4 axis modulates neuronal excitability, glial activation, synaptic plasticity, and nociceptive sensitization. Notably, this axis is frequently upregulated in both peripheral and central neurons, as well as in multiple glial populations, including astrocytes, microglia, and satellite glial cells, across diverse neuropathic pain models. Importantly, CXCR4 is one of the few chemokine receptors with a clinically approved antagonist, highlighting its unique translational potential. This review systematically summarizes the expression patterns, biological functions, and pain-related mechanisms of the CXCL12/CXCR4 axis in preclinical models of neuropathic pain and discusses current limitations and potential future therapeutic strategies targeting this pathway.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261444493"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13133439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639418","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":"Cortical mechanism of emotional pain.","authors":"Min Zhuo","doi":"10.1177/17448069251414261","DOIUrl":"10.1177/17448069251414261","url":null,"abstract":"<p><p>Most basic and clinical research on chronic pain has traditionally focused on the mechanisms and treatment of physical pain resulting from peripheral injuries in individual animals or humans. However, growing evidence highlights the importance of emotional pain, a form of distress that extends beyond the individual to include family members, partners, and friends affected by another's suffering. In this review, I summarize recent advances in animal models of empathic pain and explore cortical synaptic mechanisms underlying this form of social or emotional pain. I compare the cortical processes mediating physical pain and emotional pain, drawing on evidence from both human brain imaging and animal studies. Converging findings suggest that the anterior cingulate cortex (ACC) and insular cortex (IC) play central roles in the perception and persistence of emotional pain. Cortical potentiation appears to be a key synaptic mechanism driving long-term emotional pain, and cortical top-down modulation of spinal nociceptive transmission may help explain how emotional distress leads to abnormal somatosensory perception. Finally, the calcium-stimulated adenylyl cyclase subtype 1 (AC1) is discussed as a potential therapeutic target for the treatment of chronic pain and its associated emotional disorders.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251414261"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892751","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":"Brain networking pain and anxiety: From basic mechanism to future treatment.","authors":"Min Zhuo","doi":"10.1177/17448069251411647","DOIUrl":"10.1177/17448069251411647","url":null,"abstract":"<p><p>It is well known that pain and anxiety can enhance each other in both animals and humans. In case of chronic pain, patients often suffer anxiety and depression. Animal experiments provide important basic mechanisms for the interaction between chronic pain and anxiety. At cortical level, recent studies have consistently indicated that anterior cingulate cortex (ACC) and insular cortex (IC), two critical cortical regions for pain-related unpleasantness and suffering, are also involved in the process of emotional anxiety. At synaptic level, long-term potentiation (LTP), a key cellular mechanism for memory and chronic pain, has also been found to contribute to emotional anxiety in animal models of chronic pain. In a recent study published in <i>Neuron</i> by the group of Prof. Xu, it has been found that at subcortical level, anterior and posterior paraventricular nucleus of the thalamus (PVT) contribute to pain and anxiety through distinct projections to the basolateral amygdala (BLA) and central amygdala (CeA). In this review, I will first introduce the recent work by Prof Xu, and then discuss possible mechanisms at different levels for pain and anxiety in the condition of chronic pain, including chronic visceral pain. Some of medicines used in the current treatment will be analyzed, and potential future treatment for pain and anxiety in chronic pain conditions will be discussed.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251411647"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12764751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768712","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":"CGRP expression and signaling sensitization in a mouse model of chronic oxaliplatin-induced peripheral neuropathy.","authors":"Junwei Du, Leland C Sudlow, Margaret H Johnson, Kanishk Satish, Abraham Villagomez, Hongzhen Hu, Mikhail Y Berezin","doi":"10.1177/17448069261432028","DOIUrl":"10.1177/17448069261432028","url":null,"abstract":"<p><p>Chemotherapy-induced peripheral neuropathy (CIPN) is a frequent and dose-limiting side effect of oxaliplatin treatment, yet its molecular mechanisms remain incompletely understood. Calcitonin gene-related peptide alpha (CGRPα, encoded by <i>Calca</i>) is a neuropeptide implicated in several chronic pain conditions and has been proposed to mediate CIPN-related hypersensitivity. Here, we investigated the role of CGRPα in a mouse model of chronic oxaliplatin-induced neuropathy. Mice treated with oxaliplatin over 8 weeks developed cold allodynia and reduced sensory nerve conduction velocity, recapitulating hallmark clinical symptoms of chronic CIPN. However, contrary to expectations, we observed no increase in <i>Calca</i> mRNA expression or protein levels in the dorsal root ganglia (DRG) of male mice and a significant decrease in female mice. The proportion of CGRP-expressing neurons remained unchanged. RNA-seq revealed a two-fold upregulation of <i>Ramp1</i>, a subunit of the CGRP receptor complex. These results suggest that CGRPα signaling may be enhanced not by increased peptide expression, but rather by increased calcium-dependent release from existing neurons and increased CGRP receptor sensitization. This is consistent with known effects of oxaliplatin-induced oxidative stress, which can activate TRPA1 channels and promote calcium-dependent vesicular release of neuropeptides. Although additional validation of this model is needed, our data support a revised rationale of CGRP involvement in CIPN based on sensitization and neuropeptide release, rather than upregulation, and point to TRPA1-CGRP interactions as a potential therapeutic target in oxaliplatin-induced neuropathic pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261432028"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13018710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147308099","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":"Electroacupuncture at Zusanli (ST36) alleviates paclitaxel-induced neuropathic pain in rats via regulating TLR4 signaling pathway in the spinal cord.","authors":"Man-Ni Wang, Yuan-Xi Zhou, Yu-Xue Zhao, Jing-Wei Tan, Xiao Sang","doi":"10.1177/17448069251413879","DOIUrl":"10.1177/17448069251413879","url":null,"abstract":"<p><p>Paclitaxel (PTX) treatment induces a pathological pain state that is often associated with neuroinflammation in the central nervous system. The available interventions for PTX-induced pathological pain encounter adverse effects and limited efficacies. Recent studies have shown the significant effectiveness of Electroacupuncture (EA) in pain management as a simple and safe alternative medical treatment. Here, we evaluated the analgesic effect of EA on pain behaviors in PTX-treated rats and investigated its potential analgesic mechanisms. In this study, a pathological pain model was established in SD rats via intraperitoneal (<i>i.p</i>.) injection of PTX. EA or Sham EA treatments were applied every other day for PTX-treated rats. Pain behaviors of mechanical allodynia and thermal hyperalgesia in rats were measured, followed by analysis of the spinal cord tissue via using molecular biology methods. Here, we show that EA treatment is capable to alleviate PTX-induced mechanical allodynia and thermal hyperalgesia in rats. In addition, EA regulated the abnormal protein expression of astrocytes, microglia, neurons, TLR4-MyD88/TRIF signaling pathway and cytokines in the lumbar spinal cord of PTX-treated rats. Furthermore, we investigated the spinal co-expressions of TLR4 in astrocytes, microglia, and neurons respectively in rats and the regulatory effect of EA on TLR4 and cells mentioned above. In summary, EA shows analgesic properties as it ameliorates PTX-induced mechanical allodynia and thermal hyperalgesia probably by reducing central neuroinflammation. Therefore, we consider EA as a potential therapeutic candidate for the treatment of PTX-induced pathologic pain. Notably, this study provides the first morphological evidence that EA may concurrently influence TLR4-mediated neuroimmune interactions across multiple spinal cell types, suggesting a potential central mechanism distinct from previously reported peripheral actions.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251413879"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892773","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}