Purinergic Signalling最新文献

{"title":"Guanosine contributes to rapid purinergic regulation of dopamine during ischemia.","authors":"Moriah E Weese-Myers, Alaa S Abdelrazeq Hassan, Ashley E Ross","doi":"10.1007/s11302-026-10153-7","DOIUrl":"10.1007/s11302-026-10153-7","url":null,"abstract":"<p><p>Purinergic modulation of neurotransmission is a primary strategy employed in rapid neuroprotection during and after ischemic stroke. While the contributions of adenosine and ATP to the purinome are well-documented, guanosine-based regulatory activity has remained under-investigated. In the ischemia-vulnerable CA1 region of the hippocampus, dopamine serves as both a neurotransmitter involved in long-term potentiation during memory acquisition and as a regulator focused on modulating glutamate activity. Dopamine has been suggested as a potential protective force against glutamate-induced excitotoxicity in early ischemia. Here, we investigate changes in dopamine signaling during ischemia and demonstrate that guanosine administration during injury has an immediate protective effect. We observe rapid suppression of dopamine release following ischemic insult that is completely restored with administration of a low micromolar dose of guanosine. Changes in dopamine signaling and short-term mRNA production further suggest that guanosine's rapid regulatory role may be partially achieved through the adenosine A1 and A2a receptors and that it facilitates dopamine reuptake through the dopamine transporter DAT. We present the first evidence that guanosine plays a rapid regulatory role in dopamine neurotransmission and that it may function as a broad facilitator of neurotransmitter reuptake, diversifying our understanding of the purinome in ischemia.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 3","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13096455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of P2X7-driven purinergic signaling and NLRP3 inflammasome activation underlies the hepatoprotective effects of coenzyme Q10 against glyphosate-based herbicide exposure.","authors":"Duygu Mutluay, Seda Yakut, Gözde Yücel Tenekeci, Rüveyda Hilal Akı, Barış Denk, Adem Kara","doi":"10.1007/s11302-026-10152-8","DOIUrl":"10.1007/s11302-026-10152-8","url":null,"abstract":"<p><p>The widespread use of glyphosate-based herbicides (GBHs), including formulations such as Roundup, has raised toxicological concern due to their capacity to induce oxidative stress, inflammatory signaling, and mitochondrial dysfunction leading to hepatocellular injury. The present study investigated whether coenzyme Q10 (CoQ10) confers hepatoprotection against GBH exposure through modulation of oxidative stress-driven P2X7/NLRP3 inflammasome signaling and downstream inflammatory and apoptotic pathways. Fifty male ICR mice were randomly assigned to five groups (control, sham, CoQ10, GBH, and GBH + CoQ10) and treated by oral gavage for 49 days with Roundup (500 mg/kg/day), CoQ10 (200 mg/kg/day), or their combination. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels were assessed along with hepatic oxidative stress markers malondialdehyde (MDA), glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI). Liver injury was evaluated histologically, while proliferative and inflammatory responses were analyzed by immunohistochemistry. Hepatic expression of inflammasome- and apoptosis-related genes (P2X7, NLRP3, caspase-1, IL-1β, NF-κB, TNF-α, caspase-3, and Bcl-2) was quantified by RT-qPCR. GBH exposure markedly increased serum liver enzymes, disrupted oxidative balance, and induced necroinflammatory liver injury with Kupffer cell activation and hepatocellular nuclear alterations. These changes were associated with increased PCNA and COX-2 immunoreactivity, activation of the P2X7-NLRP3 inflammasome axis, and a proapoptotic transcriptional profile. CoQ10 coadministration attenuated biochemical, histopathological, inflammatory, and apoptotic alterations, although several parameters remained incompletely normalized. In conclusion, CoQ10 provides partial but meaningful hepatoprotection against GBH-induced liver injury, highlighting P2X7-NLRP3-linked oxidative inflammation as a key mechanism in GBH hepatotoxicity.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 3","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13091816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X7 receptor mediates the anti-tumor effect of running on cervical cancer in mice.","authors":"Hai-Yun Xiong, Rui Li, Xiu-Min Hu, Yi Zhang, Patrizia Rubini, Peter Illes, Yong Tang","doi":"10.1007/s11302-026-10143-9","DOIUrl":"10.1007/s11302-026-10143-9","url":null,"abstract":"<p><p>Previous studies have suggested that running exerts anti-tumor effects on various cancers through multiple pathways. It has been reported that the P2X7 receptor (P2X7R) may display anti-tumor activity in cervical cancer cells, and running can regulate P2X7R expression and function in mice. However, the specific impact of running on cervical cancer and whether its underlying mechanism is associated with the regulation of P2X7R levels remains to be elucidated. In this study, mice bearing U14 cervical cancer tumors were used as a model to explore the association between running and P2X7R in cervical cancer. The results showed that running significantly inhibited tumor progression in mice, accompanied by an increase in P2X7R protein expression in tumor tissues. Additionally, treatment with the P2X7R antagonist JNJ-47965567 alone or in combination with running intervention promoted tumor growth and attenuated the anti-tumor effect of running. In contrast, the P2X7R agonist BzATP alone or combined with running intervention exerted anti-tumor effects and enhanced the anti-tumor effect of running. In conclusion, the present findings suggest only a pharmacological association between P2X7R and the anti-tumor effect of running against cervical cancer progression, given that genetic validation was not performed in this study. The potential involvement of immune mechanisms remains an inference and requires further experimental validation. As a possible therapeutic target, P2X7R provides supportive data for the treatment of cervical cancer and the clinical exploration of running as an adjuvant intervention.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13083685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147691828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATP and major affective disorders: the involvement of P2X receptors in pathophysiology.","authors":"Simona Mattova, Patrik Simko, Elena Colzi, Erika Stammova, Nicol Urbanska, Maria Grigoroiu-Serbanescu, Elisabetta Coppi, Terezia Kiskova-Simkova","doi":"10.1007/s11302-026-10147-5","DOIUrl":"10.1007/s11302-026-10147-5","url":null,"abstract":"<p><p>P2X receptors, a family of ATP-gated ion channels, are increasingly recognized as key contributors to the pathophysiology of major depressive disorder. Among them, P2X7 plays a central role in stress-induced neuroinflammation by driving microglial activation, inflammasome signaling, and downstream reductions in BDNF and neuroplasticity. Additional P2X subtypes, including P2X4, further modulate neuronal and glial communication relevant to mood regulation. Evidence from animal models, human genetic studies, and early therapeutic trials supports the involvement of P2X signaling in depressive phenotypes and highlights P2X7 antagonists as promising candidates for novel antidepressant strategies. Overall, targeting P2X receptors offers a mechanistically distinct approach to understanding and treating depression.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13079264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Purinergic signaling in dengue infection: modulation of P2 receptors as a potential therapeutic strategy.","authors":"Vitória C de Melo, Kayla I de Oliveira, Marina Kipper, Margarete D Bagatini, Gilnei B da Silva","doi":"10.1007/s11302-026-10149-3","DOIUrl":"10.1007/s11302-026-10149-3","url":null,"abstract":"<p><p>Dengue is a globally widespread arboviral disease characterized by an intense inflammatory response that may progress to severe clinical manifestations, such as dengue shock syndrome and hemorrhagic fever. The lack of effective treatments underscores the urgent need to identify new therapeutic targets. In this context, purinergic signaling-mediated by molecules such as ATP and adenosine-has emerged as a central regulator of immune, inflammatory, and vascular responses during dengue virus (DENV) infection. Activation of purinergic receptors, particularly P2X7, directly influences viral replication, cytokine release, and endothelial barrier integrity, potentially contributing either to viral control or to disease severity when dysregulated. This review synthesizes the main mechanisms by which the purinergic system contributes to dengue pathogenesis, emphasizing both its physiological and pathological roles. The molecular analysis indicates that purinergic signaling plays a pivotal role in both restricting and exacerbating viral infection. Therefore, its pharmacological modulation represents a promising avenue for developing innovative therapeutic strategies, particularly for preventing severe dengue outcomes.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13046989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147594234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of purinergic receptor P2Y, G-protein coupled 2, is regulated by estrogen during the estrous cycle in mouse uterus.","authors":"Joohee Kim, Minju Kang, Byeongseok Kim, Yeonju Suh, Jimin Lee, Sangok Park, Ok-Hee Lee, Man Ryul Lee, Kwon-Ho Hong, Hoi Chang Lee, Youngsok Choi","doi":"10.1007/s11302-026-10139-5","DOIUrl":"10.1007/s11302-026-10139-5","url":null,"abstract":"<p><p>Elucidating the molecular intricacies governing uterine function is crucial for reproductive success. The purinergic receptor P2Y, G-protein coupled 2 (P2ry2), regulates critical cellular processes, and we investigated the mechanisms by which estrogen regulates P2ry2 expression in the mouse uterus using in vivo models. Uterine P2ry2 expression was analyzed across the estrous cycle in female mice using gene and protein expression analyses. To confirm hormonal regulation, ovariectomized mice were treated with β-estradiol and/or an estrogen receptor antagonist ICI 182,780. Our findings revealed a dynamic pattern of P2ry2 expression, which increased during the proestrus and estrus stages and decreased during metestrus and diestrus. P2ry2 expression was rapidly elevated following β-estradiol administration, an effect that was diminished by the estrogen receptor antagonist. This indicates that estrogen activates P2ry2 expression through estrogen receptor alpha. Additionally, P2Y2 protein was localized in the luminal epithelium and glandular epithelium. In conclusion, P2ry2 expression in the mouse uterus is tightly regulated by estrogen and is predominantly localized in the epithelial compartment, suggesting P2Y2 is closely associated with endometrial remodeling and may play a potential role in uterine tissue repair.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147582231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X7 receptor-mediated cGAS-STING pathway activation underlies chronic stress-induced depressive-like behaviors.","authors":"Xi-Meng He, Yi Zhang, Cui-Yuan Chen, Yu-Li Han Tang, Xuan Li","doi":"10.1007/s11302-026-10150-w","DOIUrl":"10.1007/s11302-026-10150-w","url":null,"abstract":"<p><p>Although chronic stress is known to trigger neuroinflammation and depressive-like behaviors, the mechanisms linking stress sensors to inflammatory cascades remain elusive. The purinergic receptor P2X7 (P2X7R), an extracellular ATP-gated cation channel primarily expressed in microglia, is a critical link between stress and neuroinflammation. While the cGAS-STING signaling pathway has been implicated in microglial reactivity, it remains unknown whether P2X7R signals via this pathway. Here, we demonstrate that chronic restraint stress in mice activates microglial P2X7R in the hippocampus, inducing mitochondrial damage. This was accompanied by activation of the cGAS-STING pathway, elevating phosphorylated STING and IRF3 levels along with pro-inflammatory cytokines. Pharmacological inhibition of P2X7R (JNJ-47965567) or STING (H-151) attenuated neuroinflammation and alleviated depressive-like behaviors. In vitro, LPS-stimulated BV2 microglia exhibited mtDNA release and cGAS-STING activation. P2X7R knockdown or pharmacological inhibition attenuated mitochondrial dysfunction, mtDNA release, and subsequent phosphorylation of STING and IRF3. In conclusion, our findings unveil a previously unrecognized mechanism in the neuroimmunological pathology of depressive-like behaviors, demonstrating that chronic stress triggers neuroinflammation through a microglial pathway involving P2X7R-mediated mitochondrial damage, mtDNA release, and cGAS-STING activation.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035991/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147582265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor growth inhibitory activity of the P2X7 receptor antagonist AZ10606120 in two cell lines of human glioblastoma.","authors":"Michela Graziano, Silvia Bono, Michela Pizzoferrato, Chiara Ferraro, Flavia Grossi, Pierluigi Navarra, Maria Martire, Lucia Lisi","doi":"10.1007/s11302-026-10144-8","DOIUrl":"10.1007/s11302-026-10144-8","url":null,"abstract":"<p><p>Glioblastoma multiforme (GBM) is among the most aggressive and lethal primary brain tumors. P2X7 is a purinergic receptor overexpressed in GBM, whose activation can promote tumor growth. Two major splice variants of the P2X7 receptor, isoforms A and B, are expressed in GBM cells. In our study, both isoforms A and B were present in GBM cells, with a slight prevalence of isoform B expression in the U87MG cell line compared to the T98G cell line. In GBM cell cultures, we evaluated the effects of P2X7 receptor activation/inhibition on cell growth. Exposure of GBM cells to various concentrations of ATP did not alter cellular activity, whereas inhibition of the P2X7 receptor with the antagonist AZ10606120, but not with A740003, significantly reduced GBM cell viability and proliferation. The U87MG cell line, which expresses the B isoform more highly, was more sensitive to the antiproliferative effects of AZ10606120. To clarify the mechanisms of AZ10606120-induced tumor inhibition, we measured the expression of proteins involved in cell repair and survival processes. AZ10606120 induced an increase in caspase-3 and p21 expression, demonstrating that P2X7R blockade can induce tumor cell death, likely by apoptosis. AZ10606120 also stimulated interleukin-6 (IL-6) release in GBM cells and induced phosphorylation of CREB and STAT3. Blockade of P2X7R by AZ10606120 appears to activate a pro-tumor IL-6/STAT3 axis. Increased IL-6 secretion and activation of the CREB and STAT3 pathways are negative prognostic signs that highlight the need to combine P2X7R inhibition with AZ10606120 with other therapies.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13031654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147532419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenosine A_2A receptors in the chorioid plexus are causal in mediating the development of hydrocephalus.","authors":"Xing-Ying Ren, Yong Tang, Peter Illes","doi":"10.1007/s11302-026-10148-4","DOIUrl":"10.1007/s11302-026-10148-4","url":null,"abstract":"<p><p>In a recent article published in Nature Communications, Zheng et al. report that heightened stimulation of A_2A receptors (A_2ARs) located in epithelial cells of the chrorioid plexus (ChP) is responsible for the development of hydrocephalus (Zheng et al., Nat Commun 17:83, 2025). They show evidence in hydrocephalus patients and mice models of hydrocephalus that the cerebrospinal fluid (CSF) concentration of adenosine is raised to about threefold of the control value. Under pathological conditions, CSF adenosine levels may be increased in response to infection, hemorrhage, traumatic insults, and tumors, all of which are known to be the initiators of hydrocephalus. In careful experiments, performed mostly in mice models, established by the injection of autologous blood (imitation of hemorrhage) or kaolin (imitation of obstruction) to the cerebral ventricles, the production of CSF, the level of adenosine, and the expression of A_2ARs was increased and in consequence the ventricles enlarged. The signaling mechanisms leading to increased production of CSF were then identified by the genetic knockdown of proteins that were assumed to be involved in this process. The A_2AR-SPAK (SPS1-related proline/alanine-rich kinase)-PI3K (phosphoinositide 3 kinase)-Akt (protein kinase B)-NF-κB (a nuclear factor)-ATP1A2 (a Na⁺,K⁺-ATPase) pathway was suggested to be instrumental in hydrocephalus development. The clinically important conclusion deriving from this observation was that A_2AR blockade by istradefylline, a Food and Drug Administration-approved drug could be introduced into the therapy of human hydrocephalus.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13013730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147514433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Light flickering with 40 Hz causes analgesia via activation of a retina-amygdala pathway and the local release of adenosine.","authors":"Wei Zhao, Yong Tang, Peter Illes","doi":"10.1007/s11302-026-10151-9","DOIUrl":"10.1007/s11302-026-10151-9","url":null,"abstract":"<p><p>In a recent article published in Cell Research, Chen et al. reported that light flickering at 40 Hz effectively counteracts chronic pain in Complete Freund Adjuvant (CFA)-treated mice and in mice whose tibial and common peroneal nerves were ligated (spared nerve injury, SNI) [1]. These mice served as models for inflammatory and neuropathic pain, respectively. After establishing that 40 Hz light flickering exerted analgesia in both pain models, a systematic search started for the neuronal pathways involved and the conditions required for this effect. The combination of retrograde and anterograde tracing techniques indicated that retinal ganglion cells (RGCs) project monosynaptically to the central amygdala (CeA), and chemogenetic or optogenetic activation of this pathway simulates the effects of 40 Hz light stimulation. Genetic sensors for adenosine expressed in the CeA proved that such a light stimulation caused an increase in the local concentration of adenosine, via the promotion of the equilibrative adenosine transporter-mediated outflow of the nucleoside from CNS cells. The enriched adenosine levels apparently stimulated A_2A receptors (Rs) as proved by the abolition of 40 Hz light flickering-induced analgesia by pharmacological blockade of A_2ARs, or their genetic knockdown/knockout. The target neurons in the CeA were identified as belonging to the proenkephalin-containing type; their selective ablation abolished the effect of light stimulation. Finally, two capsaicin injections, 3 h apart, the second one either combined with saline or the protein synthesis inhibitor anisomycin, showed that anisomycin deleted chronic pain memory traces. Hence, 40 Hz light flickering may be a non-pharmacological manipulation for alleviating chronic pain in humans, without the cardiovascular and CNS side effects inherent to systemic adenosine application.</p>","PeriodicalId":20952,"journal":{"name":"Purinergic Signalling","volume":"22 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13013863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147514455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}