Vascular pharmacology最新文献

{"title":"Explosive discovery, surprising future: The extraordinary journey of nitroglycerin, nitroderivatives and nitric oxide","authors":"Maria Rosa Montinari ,&nbsp;Sergio Minelli ,&nbsp;John D. Horowitz ,&nbsp;Raffaele De Caterina","doi":"10.1016/j.vph.2025.107517","DOIUrl":"10.1016/j.vph.2025.107517","url":null,"abstract":"<div><div>For over 150 years, nitrates have been a cornerstone in the treatment of cardiovascular disease. Nitroglycerin — synthesized by Italian chemist Ascanio Sobrero in 1847 — was initially used in explosives, as the main component of dynamite, by Alfred Nobel. The Scottish physician Lauder Brunton first used amyl nitrite for angina in 1867, and in 1879 the English physician William Murrell described the benefits of nitroglycerin for angina pectoris. Organic nitrates, including nitroglycerin, act as nitric oxide donors, sharing the mechanism of NO release, which induces vasodilation. This paper reviews the fascinating history of nitroglycerin and nitroderivatives, the related discovery of nitric oxide as a cardiovascular signaling molecule, and the 1998 Nobel Prize awarded for this discovery. The paper also succinctly explores current and future roles of nitric oxide donors in cardiovascular treatment.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107517"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144470863","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":"Exploring new cardiovascular frontiers: The Italian cardiovascular research landscape","authors":"Rosalinda Madonna ,&nbsp;Vincenzo Lionetti","doi":"10.1016/j.vph.2025.107525","DOIUrl":"10.1016/j.vph.2025.107525","url":null,"abstract":"","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107525"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144709174","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":"Macrophage and cardiomyocyte roles in cardioprotection: Exploiting the NLRP3 Inflammasome inhibitor INF150","authors":"Magalì Giordano ,&nbsp;Saveria Femminò ,&nbsp;Federica Blua ,&nbsp;Francesca Boccato ,&nbsp;Chiara Rubeo ,&nbsp;Beatrice Mantuano ,&nbsp;Francesca Cioffi ,&nbsp;Stefano Comità ,&nbsp;Arianna Brovero ,&nbsp;Rosa Ciullo ,&nbsp;Massimo Bertinaria ,&nbsp;Claudia Penna ,&nbsp;Pasquale Pagliaro","doi":"10.1016/j.vph.2025.107487","DOIUrl":"10.1016/j.vph.2025.107487","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular diseases remain the leading cause of disability and death in the Western world. Effective cardioprotection involves limiting ischemia/reperfusion injury (IRI), including cell death (pyroptosis) driven by the NLRP3 inflammasome. While various cardiac resident cellular populations contribute to cardioprotection, it remains unclear whether targeting resident macrophages is inherently cardioprotective. Given that INF150, an NLRP3 inhibitor, exhibits varying abilities to penetrate cardiomyocytes and macrophages, we sought to address this question.</div></div><div><h3>Methods</h3><div>We studied the cardioprotective potential of INF150, the potent metabolite of the NLRP3 inhibitor INF195, in isolated hearts or cells. In isolated hearts, we measured infarct size, caspase-1 cleavage, and interleukins (IL) release, while in macrophages, naïve H9c2 and differentiated H9c2 cells, we analyzed cell viability, and pyroptosis markers, including IL-1β release and Gasdermin D cleavage, following hypoxia/reoxygenation (H/R).</div></div><div><h3>Results and conclusion</h3><div>While INF150 effectively shielded macrophages from LPS/ATP challenges, it failed to penetrate H9c2 and differentiated H9c2, even at high concentrations (no changes in pyroptosis markers induced by H/R). In the isolated mice heart model, INF150 did not demonstrate cardioprotective effects: infarct size, IL-1β, cleaved caspase-1 levels did not change significantly across tested concentrations of INF150. These findings suggest that while INF150 shows promise in macrophage/phagocytic models, its inability to penetrate cardiomyocytes limits its effectiveness in the whole cardiac tissue. Our results underscore the importance of cardiomyocyte uptake for effective cardioprotection, highlighting the need for NLRP3 inhibitors capable of targeting these cells directly. Future research should focus on enhancing the delivery and cardiomyocyte uptake of NLRP3 inhibitors to achieve cardioprotection. Unlike its precursor, INF195, which penetrates H9c2 cells, INF150 does not appear to offer cardioprotection in the whole organ.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107487"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651055","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":"Pharmacological activation of NO-sensitive guanylyl cyclase ameliorates obesity-induced arterial stiffness","authors":"Enkhjargal Budbazar ,&nbsp;Aylin Balmes ,&nbsp;Danielle Elliott ,&nbsp;Lisette Peres Tintin ,&nbsp;Timo Kopp ,&nbsp;Susanne Feil ,&nbsp;Robert Feil ,&nbsp;Tilman E. Schäffer ,&nbsp;Francesca Seta","doi":"10.1016/j.vph.2025.107503","DOIUrl":"10.1016/j.vph.2025.107503","url":null,"abstract":"<div><h3>Background &amp; purpose</h3><div>Arterial stiffness, or loss of elastic compliance in large arteries, is an independent precursor of cardiovascular disease (CVD) [<span><span>1</span></span>] and dementia [<span><span>2</span></span>] for which currently there are no targeted therapies. We previously discovered that decreases in NO-sensitive guanylyl cyclase (NO-GC), the NO receptor which synthesizes cGMP, and in its target vasodilator-stimulated phosphoprotein (pVASP^S239), lead to increased cytoskeletal actin polymerization in vascular smooth muscle cells (VSMCs) contributing to increased arterial stiffness [<span><span>3</span></span>]. In the current study, we tested whether activating NO-GC with an NO-GC activator (cinaciguat) modulates pVASP^S239 and cytoskeletal actin polymerization in VSMCs, thereby preventing obesity-induced arterial stiffness<em>.</em></div></div><div><h3>Experimental approach &amp; key results</h3><div>Cinaciguat administration (5 mg/kg) to high fat, high sucrose diet (HFHS)-fed mice, our established model of arterial stiffness [<span><span>4</span></span>], (1) decreased pulse wave velocity, the in vivo index of arterial stiffness, without affecting blood pressure; (2) increased aortic pVASP^S239 levels; and (3) decreased actin polymerization, measured as ratio of filamentous (F) to globular (G) actin, compared to vehicle administration. In cultured VSMCs, cinaciguat (10 μmol/L) increased pVASP^S239 levels and decreased the F/G actin ratio at baseline and after stimulation with the cytokine tumor necrosis factor α (TNFα), which we previously showed is significantly increased in the aorta of HFHS-fed mice [<span><span>[4]</span></span>, <span><span>[5]</span></span>, <span><span>[6]</span></span>]. These effects were abrogated in aortas and VSMCs from mice with smooth muscle-specific cGKI deletion (cGKI^SMKO), while being mimicked by a cell-permeable cGMP analog (8-Br-cGMP), which also decreased VSMC stiffness in vitro.</div></div><div><h3>Conclusions &amp; implications</h3><div>Collectively, our data strongly support the notion that pharmacological NO-GC activation would be beneficial in decreasing obesity-associated arterial stiffness by decreasing VSMC cytoskeletal actin hyper-polymerization. If translated to humans, NO-GC activators could become a viable approach to clinically treat arterial stiffness, which remains an unmet medical need.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107503"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144095155","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":"Single-cell RNA sequencing (scRNA-seq) and its insights into cellular heterogeneity in atherosclerosis","authors":"Baixue Yu ,&nbsp;Miron Sopic ,&nbsp;Judith C. Sluimer","doi":"10.1016/j.vph.2025.107499","DOIUrl":"10.1016/j.vph.2025.107499","url":null,"abstract":"<div><div>Single-cell RNA sequencing (scRNA-seq) has transformed our understanding of cellular diversity in human biology, providing novel insights into disease mechanisms. In cardiovascular disease (CVD), scRNA-seq enables precise mapping of complex cell populations, uncovering unique cell types and states that influence disease progression and suggest new therapeutic targets. In atherosclerosis (AS), scRNA-seq has redefined plaque pathology by identifying distinct cell types, including endothelial cells (ECs), smooth muscle cells (SMCs), fibroblasts, macrophages, T cells, and B cells, each with specific roles in plaque stability, inflammation, and disease progression. In our review, we summarized these major cellular populations and their cellular heterogeneity in non-diseased and atherosclerotic aorta, as identified by scRNA-seq in mice and human tissues. We discussed conserved and species-specific subpopulations, their defining markers, and their functional implications in plaque progression. In addition, we integrated findings from scRNA-seq with experimental studies to highlight key molecular targets with therapeutic potential. In the future, these insights offer a refined cellular and molecular framework of atherosclerosis and may help the development of targeted interventions to promote plaque stabilization and reduce cardiovascular risk.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107499"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144040035","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":"Survivin in cardiovascular diseases and its therapeutic potential","authors":"Thomas Mousso ,&nbsp;Khanh Pham ,&nbsp;Rhonda Drewes ,&nbsp;Sefunmi Babatunde ,&nbsp;Jessica Jong ,&nbsp;Alanna Krug ,&nbsp;Gabrielle Inserra ,&nbsp;John Biber ,&nbsp;Joseph A. Brazzo ,&nbsp;Sachin Gupte ,&nbsp;Yongho Bae","doi":"10.1016/j.vph.2025.107475","DOIUrl":"10.1016/j.vph.2025.107475","url":null,"abstract":"<div><div>Aberrant changes in cell behaviors, such as proliferation, apoptosis, and migration, are some of the contributing factors to the development of various cardiovascular diseases (CVDs) and pathologies, including atherosclerosis, neointimal hyperplasia, and heart failure. In recent years, numerous studies have identified survivin, a key player in the anti-apoptotic pathway, to be extensively involved in modulating cellular functioning in cancer, with many reaching clinical trials. Though seemingly different, CVDs and cancer share abundant similarities regarding abnormal cell modifications and behaviors. This overlap has sparked growing interest in investigating survivin as a therapeutic target in the context of CVD. With new findings emerging rapidly, a comprehensive understanding of survivin's role in cardiovascular pathology is crucial to revealing its full therapeutic potential and translating these discoveries into effective treatments. This review discusses recent findings of survivin in CVDs and related pathologies, focusing on its dual role in promoting proliferation and inhibiting apoptosis, specifically in atherosclerosis, neointimal hyperplasia, stroke, hypertension, myocardial infarction, and heart failure. Across different cell types and pathological contexts, survivin plays a pivotal role throughout the disease progression–from the onset of disease development to the facilitation of compensatory mechanisms post-injury–primarily through its function in regulating cell proliferation and apoptosis. Furthermore, given the limited research on survivin as a therapeutic target for CVDs, potential clinical avenues, including YM155 (a survivin inhibitor) or adenoviral, adeno-associated, and lentiviral vectors, are also discussed. Overall, this review highlights survivin as a promising target for mitigating the detrimental effects of CVDs and to provide new perspectives to advance research on the intervention of CVDs and associated pathologies.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107475"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143508341","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":"Exploring the interplay between valvular and serum zinc and copper levels and disease markers in aortic stenosis","authors":"Bartłomiej Perek ,&nbsp;Piotr Rzymski ,&nbsp;Aleksandra Proch ,&nbsp;Mateusz Puślecki ,&nbsp;Barbara Poniedziałek ,&nbsp;Andrzej Fal ,&nbsp;Anna Komosa ,&nbsp;Marek Jemielity ,&nbsp;Przemysław Niedzielski","doi":"10.1016/j.vph.2025.107497","DOIUrl":"10.1016/j.vph.2025.107497","url":null,"abstract":"<div><div>Aortic stenosis (AS) is a progressive condition characterized by valve calcification and significant morbidity, often requiring invasive intervention. The AS pathophysiology is multifaceted, with evidence suggesting a role for trace elements. However, whether zinc (Zn) and copper (Cu) are associated with valve calcification is unclear. This exploratory study assessed the Zn and Cu levels in the serum and aortic valves of AS patients undergoing surgical valve replacement and explored the relationships between trace elements and clinical and biochemical parameters to better understand their potential roles in AS pathophysiology. An inverse relationship was observed between serum Zn levels and systolic pressure gradients across the valve (<em>p</em> &lt; 0.0001). Zn accumulation was identified in calcified aortic valves, suggesting a systemic redistribution of Zn during disease progression. The valvular Cu/Zn ratio was reversed (&lt;1) compared to that in serum. The lipoprotein(a), an inflammatory marker, was positively correlated with serum Cu levels (<em>p</em> = 0.0007) and the Cu/Zn ratio (<em>p</em> = 0.02). However, no direct association was found between valvular Cu content and the AS severity. The findings suggest that Zn depletion in serum, coupled with its accumulation in calcified valves, reflects a disease-driven redistribution mechanism that may serve a protective role against calcification progression. Additionally, the study highlights a potential interplay between Cu metabolism and inflammatory processes in AS. Further research is required to determine whether therapeutic modulation of Zn levels could offer benefits in AS management.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107497"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870747","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":"Efficacy of beta-blocker agents on clinical outcomes in patients with thoracic aortic aneurysm: A systematic review and meta-analysis of randomized controlled trials","authors":"Lokman H. Tanriverdi ,&nbsp;Annie Barrett ,&nbsp;Asanish Kalyanasundaram ,&nbsp;Mohammad A. Zafar ,&nbsp;Bulat A. Ziganshin ,&nbsp;John A. Elefteriades","doi":"10.1016/j.vph.2025.107494","DOIUrl":"10.1016/j.vph.2025.107494","url":null,"abstract":"<div><h3>Objective</h3><div>Studies investigating the efficacy of β-blocker agents for patients with thoracic aortic aneurysm (TAA) have produced heterogeneous and conflicting results. We assess the effects of β-blockers on clinical outcomes in patients with TAA.</div></div><div><h3>Methods</h3><div>A systematic literature search was performed through Ovid MEDLINE, EMBASE, Web of Science, Pubmed and Cochrane CENTRAL, all from inception to April 30, 2024. Randomized controlled trials (RCTs) exploring the effect of β-blocker agents in patients with TAA were considered for inclusion, with no population restriction. Inverse variance–weighted random-effects model was used. The overall risk of bias assessment was conducted by Cochrane Risk of Bias 2 tool. The primary outcome was aortic events during follow-up.</div></div><div><h3>Results</h3><div>We included a total of 161 patients with TAA (mean age, 27.6 years; 80 [49.7 %] male, mean follow-up 6.7 years) in 4 RCTs. The pooled risk ratio in the β-blocker arm for aortic events was 0.74 [95 % CI (0.20; 2.71), I²: 0 %, <em>p</em> = 0.64, low certainty of evidence (CoE)] when compared to placebo or no treatment in patients with TAA. The pooled risk ratios for aortic dissection or death (all-cause mortality) or in the β-blocker arm were 0.45 (95 % CI (0.10; 1.98), I²: 0 %, <em>p</em> = 0.29, low CoE) and 0.58 (95 % CI (0.15; 2.24), I²: 0 %, <em>p</em> = 0.43, low CoE), respectively. The risks of aortic dissection, rupture, or death were comparable, regardless of agent, disease, and age.</div></div><div><h3>Conclusion</h3><div>We found no evidence of benefit from β-blocker treatment for patients with TAA. More robust RCTs are needed to establish evidence-based recommendations.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107494"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807712","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":"Cdc42 is crucial for mural cell migration, proliferation and patterning of the retinal vasculature","authors":"Alberto Álvarez-Aznar ,&nbsp;Malavika Desai ,&nbsp;Michael M. Orlich ,&nbsp;Elisa Vázquez-Liébanas ,&nbsp;Ralf H. Adams ,&nbsp;Cord Brakebusch ,&nbsp;Konstantin Gaengel","doi":"10.1016/j.vph.2025.107472","DOIUrl":"10.1016/j.vph.2025.107472","url":null,"abstract":"<div><h3>Aims</h3><div>Mural cells constitute the outer lining of blood vessels and are essential for vascular development and function. Mural cell loss or malfunction has been associated with numerous diseases including diabetic retinopathy, stroke and amyotrophic lateral sclerosis. In this work, we investigate the role of CDC42 in mural cells <em>in vivo</em>, using the developing mouse retina as a model.</div></div><div><h3>Methods</h3><div>In this study, we generated a mouse model for <em>Cdc42</em> deletion in mural cells by crossing <em>Pdgfrb-CreER</em>^<em>T2</em> mice with <em>Cdc42flox/flox</em> mice. This model (<em>Cdc42</em>^{<em>iΔMC</em>}) allowed us to investigate the role of CDC42 in pericytes and smooth muscle cells in the developing and adult retinal vasculature.</div></div><div><h3>Results</h3><div>We find that, during postnatal development, CDC42 is required in both, pericytes and smooth muscle cells to maintain proper cell morphology, mural cell coverage and distribution. During retinal angiogenesis, <em>Cdc42</em>-depleted pericytes lag behind the sprouting front and exhibit decreased proliferation. Consequently, capillaries at the sprouting front remain pericyte deprived, become dilated and are prone to increased vascular leakage. In addition, arteries and arterioles deviate from their normal growth directions and trajectory. While in the adult retina, mural cell coverage normalizes and pericytes adopt a normal morphology, smooth muscle cell morphologies remain abnormal and arteriolar branching angles are markedly reduced.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrate that CDC42 is required for mural cell migration and proliferation and suggest that mural cells are essential for normal morphogenesis and patterning of the developing retinal vasculature.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107472"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459673","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":"Vasorelaxant effects of 3-methoxycatechol are not via direct activation of voltage-gated potassium channels","authors":"Rían W. Manville ,&nbsp;Samuel N. Baldwin ,&nbsp;Olivia H. Schaub ,&nbsp;Thomas A. Jepps ,&nbsp;Geoffrey W. Abbott","doi":"10.1016/j.vph.2025.107471","DOIUrl":"10.1016/j.vph.2025.107471","url":null,"abstract":"","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107471"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400355","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}