Molecular Pain最新文献

{"title":"The butterfly effect and its electrical mechanism: Non-linear non-reciprocate sawtooth subthreshold oscillations deactivate nociceptors.","authors":"M Danilo Boada","doi":"10.1177/17448069251391016","DOIUrl":"10.1177/17448069251391016","url":null,"abstract":"<p><p>Across mammalian evolution, chronic pain has no adaptive value, and in the wild, there's no evidence of its existence. Since rodents are often used to model chronic pain in humans, the question of how the peripheral somatosensory system of these animals responds to injury becomes critical to our overall translatability efforts. Over a decade of intensive work on this question has led to the discovery of the primordial systemic process that protects the mammalian peripheral somatosensory system against uncontrolled hyperexcitability, as well as its underlying electrical mechanism. Named the \"butterfly effect,\" this two-stage process enables the appropriate animal behavioral response to injury (first stage) while evading pathology by deactivating hyperactive nociceptive neurons (second stage). This deactivation process involves the generation of subthreshold membrane sawtooth oscillations, which, rather than producing ectopic discharges, lead the cells to a quiescent state. The complex nature of this phenomenon challenges any simplistic approach to modeling and translating animal pain physiology directly into human pain pathology.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251391016"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12705952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355236","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":"Single cell transcriptomic analysis reveals dynamic cellular composition changes at acupuncture point BL23 (Shenshu) in low back pain.","authors":"Gexin Zhao, Xiuju Wu, Shunfa Huang, Shihui Huang, Guodong Zhang, Xin Zhou, Shengqi Cao, Hyun-Ju Lim, Mark I Ii Duhon, Rui Li, Kristina I Boström, Xinmin Li","doi":"10.1177/17448069251405974","DOIUrl":"10.1177/17448069251405974","url":null,"abstract":"<p><p>The cellular and molecular mechanisms of acupuncture have been investigated across various tissues in multiple animal models. However, the dynamic cellular and molecular changes at human acupuncture points remain unexplored. The primary challenge preventing such a study is the practical difficulty of obtaining sufficient cells from acupoints. To address this, we developed a new needle manipulation technique that enables the collection of sufficient cell number from the acupuncture needle during the treatment. Using this approach and single-cell technology, we identified eight cell types at the acupoint BL23: inflammatory fibroblast, myofibroblast, skeletal muscle cell, endothelial cell, smooth muscle cell, adipocyte, macrophage, and a novel cell type characterized by marker genes <i>CNTNAP2</i> and <i>CSMD1</i>. Remarkably, this novel cell population was significantly enriched during the pain relief phase compared to the pain state, while the other seven cell types were significantly reduced following acupuncture analgesia. Transcriptomic analysis suggested that these novel cells are involved in synapse assembly and synaptic plasticity. This study presents the first characterization of cellular and transcriptional dynamics at the acupoint BL23, offering new insights into the mechanism underlying acupuncture-induced pain relief.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251405974"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12743158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145636250","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 reduces visceral pain and anxiety associated with inflammatory bowel disease by inhibition of vHPC-to-mPFC pathway.","authors":"Xue-Fei Hu, Wen-Qiang Ge, Teng-Fei Hou, Pan-Pan Lv, Fan Wu, Qiang Fu, Qi-Shun Lin, Li-Xue Lin, Hong Zhang, Li-Jun Zhang, Hong-Chun Xiang, Shu-Xiu Zhu, Man Li","doi":"10.1177/17448069251396875","DOIUrl":"10.1177/17448069251396875","url":null,"abstract":"<p><p>EA effectively treats gastrointestinal diseases, pain symptoms, and emotional disorder. Furthermore, vHPC and mPFC are two of the crucial nuclei involved in controlling chronic pain and anxiety-like behaviors. In the present study, it is investigated whether EA may reduce visceral pain and anxiety associated with inflammatory bowel disease (IBD) by inhibition of vHPC-to-mPFC pathway. We found that EA alleviated visceral hyperalgesia and anxiety in TNBS-treated IBD mice. EA decreased the numbers of c-Fos and neurogranin (labeled glutamatergic neurons) co-labeled neurons in both vHPC and mPFC. EA suppressed the activation of vHPC and mPFC pyramidal neurons associated with anxiety-like behaviors and EA suppressed the activation of vHPC neuronal response to von Frey filament. In addition, chemogenetic inhibition of the vHPC-to-mPFC pathway alleviated mechanical allodynia, visceral hyperalgesia and anxiety in IBD mice. However, chemogenetic activation of vHPC-to-mPFC pathway antagonized the effect of EA on anxiety and visceral hyperalgesia, but not on mechanical allodynia in IBD mice. In conclusion, our findings revealed that vHPC-to-mPFC pathway is involved in the inhibitory effect of EA on anxiety and pain sensitivity in IBD mice. EA may exert anti-anxiety effect via inhibition of vHPC-to-mPFC pathway. Thus, our study provides new information about the cellular circuits mechanisms of the therapeutic effect of EA on the comorbidity of visceral pain and anxiety induced by IBD.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251396875"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12665826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145445439","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}

{"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":"Humanized anti-P2X4 scFv reduces ATP-induced P2X4 currents and modulates excitability in human DRG neurons.","authors":"Nesia A Zurek, Mark W Shilling, Jenna B Demeter, Reza Ehsanian, Ian M Adams, Aleyah E Goins, Sachin Goyal, Philippe Séguéla, June Bryan I de la Peña, Adinarayana Kunamneni, Karin N Westlund, Sascha Ra Alles","doi":"10.1177/17448069251376200","DOIUrl":"10.1177/17448069251376200","url":null,"abstract":"<p><p>Chronic pain affects nearly 100 million adults in the U.S., yet few novel therapeutics have emerged in recent decades. P2X4 receptor (P2X4R), implicated in pain signaling, represents a promising target. We evaluated a humanized single-chain variable fragment (hscFv) targeting P2X4R for its ability to reduce ATP-induced currents and modulate excitability in human dorsal root ganglion (hDRG) neurons. Voltage-clamp recordings confirmed that human P2X4R (hP2X4R) hscFv significantly reduced ATP-evoked currents in HEK-293T cells expressing human P2X4, likely by relocalization of the receptor to the perinuclear region after hscFv treatment. Immunohistochemistry and transcriptomic analyses demonstrated widespread P2X4R (<i>P2RX4</i>) expression across hDRG neuronal subtypes in both male and female donors. Current-clamp recordings revealed that hP2X4R hscFv selectively increased action potential (AP) threshold in multi-firing hDRG neurons, without affecting single-firing neurons. Spontaneous activity at rest and depolarizing spontaneous fluctuation (DSF) amplitude were also reduced. Analysis confirmed consistent effects of hP2X4R hscFv on excitability parameters. These findings suggest that hP2X4 hscFv exerts modest but targeted effects on human sensory neurons, supporting its potential as a novel therapeutic for chronic pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251376200"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12446818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144962172","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":"Analgesia and silymarin: What are the opportunities and challenges?","authors":"Mehdi Dehghani Firoozabadi, Behrang Nooralishahi, Fatemeh Rezaei-Tazangi","doi":"10.1177/17448069251377460","DOIUrl":"10.1177/17448069251377460","url":null,"abstract":"<p><p>Pain is an unpleasant sensory and emotional sensation about actual or possible tissue damage that can cause remarkable health and economic problems. For pain relief, analgesic drugs are commonly utilized; however, their prolonged use can cause different side effects from mild to severe stages. Therefore, discovering new and alternative choices for analgesic purposes is of importance. Hopeful evidence has shown that flavonoid compounds have various therapeutic and pharmacological potentials. Among these, silymarin, obtained from the milk thistle plant <i>Silybum marianum</i>, has addressed its competence in medicine, as demonstrated by its capacity against metabolic diseases, malignancies, inflammatory-related disorders, and organ toxicities. In the recent decade, some documents have stated the analgesic influences of silymarin, especially in some pathological situations like rheumatoid arthritis and neuropathic pain. Also, there is promising information regarding the possible synergistic effects of silymarin and some pharmacological or bioactive compounds. For these reasons, this narrative literature review aims to summarize and discuss the analgesic abilities of this flavonoid agent in pathological and nonpathological conditions and its interactions with other drugs with a focus on the involved mechanisms.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251377460"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12464410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144962108","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":"MBD1-dependent recruitment of SUV39h1 induces H3K9me3-mediated transcriptional silencing of <i>Oprm1</i> in dorsal root ganglia after peripheral nerve injury.","authors":"Hengwei Sheng, Hualei Gong, Xiaolin Liu, Wenbo Wu, Helena Soares da Silva, Sen Huang, Kai Mo","doi":"10.1177/17448069251389416","DOIUrl":"10.1177/17448069251389416","url":null,"abstract":"<p><p>The downregulation of mu-opioid receptor (MOR) expression in dorsal root ganglia (DRG) following peripheral nerve injury plays a pivotal role in neuropathic pain development and contributes to the reduced efficacy of morphine analgesia. The molecular mechanisms underlying this transcriptional silencing remain poorly understood. In this study, we demonstrate that peripheral nerve injury induces upregulation of methyl-CpG-binding domain protein 1 (MBD1) and histone lysine methyltransferase SUV39H1, leading to increased trimethylation of histone H3 at lysine 9 (H3K9me3) at the <i>Oprm1</i> gene locus in injured DRG neurons. Genetic ablation of MBD1 reversed injury-induced MOR downregulation at both mRNA and protein levels, attenuated H3K9me3 enrichment at the <i>Oprm1</i> promoter, and alleviated neuropathic pain behaviors, despite persistent SUV39H1 upregulation. Mechanistic studies revealed that nerve injury enhances the recruitment of SUV39H1 and H3K9me3 to the <i>Oprm1</i> promoter, which is dependent on MBD1. Our findings establish a novel epigenetic mechanism wherein MBD1-mediated recruitment of SUV39H1 promotes H3K9me3-dependent transcriptional silencing of <i>Oprm1</i> in DRG neurons following peripheral nerve injury.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251389416"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12618850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145293100","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":"Gut microbiota-derived short-chain fatty acid suppresses the excitability of rat nociceptive secondary neurons via G-protein-coupled receptor 41 signaling.","authors":"Yukito Sashide, Mamoru Takeda","doi":"10.1177/17448069251320233","DOIUrl":"10.1177/17448069251320233","url":null,"abstract":"<p><p>Short-chain free fatty acids (SCFAs) are generated by gut microbiota through anaerobic fermentation of dietary fibers. Although gut microbiota-derived SCFAs modulate voltage-gated Ca²⁺ channels via G-protein-coupled receptor 41 (GPR41) in isolated sympathetic ganglion neurons, the influence of SCFAs, specifically propionic acid (PA), on the excitability of nociceptive neurons under in vivo conditions has yet to be ascertained. In the current study we assessed whether systemic PA administration diminishes the excitability of nociceptive trigeminal spinal nucleus caudalis (SpVc) wide-dynamic range neurons responding to mechanical stimulation. Extracellular single-unit recordings from SpVc wide-dynamic range neurons were performed in anesthetized rats after mechanical stimulation of the orofacial region. PA significantly and reversibly inhibited the mean firing frequency of SpVc neurons in response to both non-noxious and noxious mechanical stimuli in a dose-dependent manner. Simultaneous administration of a GPR41 inhibitor abolished the PA-induced inhibited firing rate of SpVc neurons, indicating that systemic PA decreased the excitability of nociceptive secondary trigeminal neurons by activating GPR41 signaling-mediated inhibition of voltage-gated Ca²⁺ channels in the central terminals of the SpVc. Modulation of trigeminal nociception by systemic SCFA administration indicates that gut microbiota-derived SCFAs could be effective analgesic agents for relieving trigeminal pain, creating a new therapeutic strategy for the management of trigeminal pain, including clinical pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251320233"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374460","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":"AMPK activation mitigates inflammatory pain by modulating STAT3 phosphorylation in inflamed tissue macrophages of adult male mice.","authors":"Hongchun Xiang, Yuye Lan, Liang Hu, Renjie Qin, Hongping Li, Tao Weng, Yan Zou, Yongmin Liu, Xuefei Hu, Wenqiang Ge, Hong Zhang, Hui-Lin Pan, Na-Na Yang, Wentao Liu, Guowei Cai, Man Li","doi":"10.1177/17448069251321339","DOIUrl":"10.1177/17448069251321339","url":null,"abstract":"<p><p>Inflammatory pain presents a significant clinical challenge. AMP-activated protein kinase (AMPK) is recognized for its capacity to alleviate inflammation by inhibiting transcription factors such as nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription (STAT). Our prior research demonstrated that AMPK reduces inflammatory pain by inhibiting NF-κB activation and interleukin-1 beta (IL-1β) expression. However, the role of AMPK in regulating reactive oxygen species (ROS) and inducible nitric oxide synthase (iNOS) by modulating STAT3 phosphorylation in inflammatory pain remains inadequately understood. This study aims to investigate the role of AMPK in modulating STAT3 phosphorylation in the macrophages of inflamed tissues to mitigate inflammatory pain. A Complete Freund's Adjuvant (CFA)-induced inflammatory pain model was established by subcutaneous injection into the plantar surface of the left hindpaw of adult male mice. Behavioral tests of mechanical allodynia and thermal latency were used to determine nociceptive behavior. Immunoblotting quantified p-AMPK and iNOS expression levels. Nuclear translocation of p-STAT3(Ser727) and STAT3 in macrophages was assessed by western blot and immunofluorescence. ROS accumulation and mitochondrial damage in NR8383 macrophages were detected by flow cytometry. Lentivirus infection cells experiment was performed to transfect vectors encoding the STAT3 S727D mutants. Treatment with the AMPK activator AICAR alleviated CFA-induced inflammatory pain, enhanced AMPK phosphorylation, and reduced iNOS expression in inflamed skin tissues. AICAR effectively prevented STAT3 nuclear translocation while promoting the phosphorylation of STAT3 (Ser727) in the cytoplasm. In vitro studies with CFA-stimulated NR8383 macrophages revealed that AICAR increased STAT3(Ser727) phosphorylation, curtailed iNOS expression, and attenuated ROS accumulation and mitochondrial damage. Furthermore, the S727D mutation, which enhances STAT3 phosphorylation, replicated the protective effects of AICAR against CFA-induced oxidative stress and mitochondrial dysfunction. Our study shows that the AMPK acitvation downregulates iNOS expression by inhibiting the STAT3 nuclear translocation and promotes cytoplasmic STAT3(Ser727) phosphorylation, which reduces ROS expression and mitochondrial dysfunction, thereby alleviating inflammatory pain. These findings underscore the therapeutic potential of targeting AMPK and STAT3 pathways in inflammatory pain management.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251321339"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374457","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}