Journal of Cardiovascular Pharmacology最新文献

{"title":"Sodium-glucose transporter-2 inhibitors: safety and efficacy in patients with peripheral artery disease.","authors":"Katelyn J Galli, Mark Wadid, Youssef Bessada","doi":"10.1097/FJC.0000000000001703","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001703","url":null,"abstract":"<p><p>The objective of this review is to assess the safety and efficacy of sodium-glucose cotransporter-2 inhibitors (SGLT-2is) in patients with peripheral arterial disease (PAD). A literature search of PubMed and EMBASE databases (through March 2025) was performed with MeSH words and phrases related to SGLT-2is AND PAD. Articles encompassing original research including results specifying safety and efficacy outcomes particularly in the PAD population were included. Narrative reviews or studies with lack of a substantial PAD population or relevant outcomes were excluded. Our literature search resulted in 289 articles of which 18 were included in the current review. Findings consistently highlighted the cardiovascular benefits SGLT-2is show in PAD patients, supporting their potential role in improving clinical outcomes. Most studies showed neutral or favorable safety regarding lower limb events, suggesting no more risk of adverse limb-related outcomes compared to the non-PAD population. Patients with PAD are likely to see improved outcomes and favorable safety with SGLT-2is, namely, canagliflozin, empagliflozin, and dapagliflozin. Observation of specific PAD populations also suggests that there is no higher risk of adverse limb events, including amputation risk, as compared to patients without PAD. Literature supports the safe and effective use of SGLT-2is in patients with concomitant PAD, regardless of the indication for use. Ongoing studies are needed to assess specific PAD outcomes with SGLT-2is and determine the specific mechanisms proposed for such benefits.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart Rate Lowering with Ivabradine and Burden of Symptoms in Patients with Postural Orthostatic Tachycardia Syndrome.","authors":"Michele Marchetta, Rocio I Lopez, Austin C Hogwood, Georgia Thomas, Gerardina Abbate, Roshanak Markley, Justin M Canada, Antonio Abbate","doi":"10.1097/FJC.0000000000001705","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001705","url":null,"abstract":"<p><p>Postural Orthostatic Tachycardia Syndrome (POTS) is a clinical syndrome of tachycardia upon standing leading to palpitations, dizziness, chest pain and/or fatigue. An exaggerated norepinephrine response with standing is often present in POTS, but it remains unclear whether the tachycardia is compensatory for a reduced stroke volume or whether the tachycardia is itself causing the symptoms of POTS. We herein report the effects of heart rate lowering with ivabradine, a selective If channel blocker, on symptom burden in patients with POTS. Following ivabradine treatment, there was a significant reduction in the change in heart rate with standing (ΔHR) in all patients from 40 (30-70) to 15 (8-19) bpm (p=0.011), without significant changes in blood pressure. The Malmö score was significantly reduced in all patients from 86 (74-92) to 39 (32-66) (p=0.005). A correlation between ΔHR and the change in Malmö score (R=+0.828; R2 quadratic= 0.635; p<0.001) was present. The parallel improvement in heart rate response and symptoms with ivabradine suggests that the tachycardia response in POTS may not be considered compensatory but rather central to the pathophysiology of POTS symptoms.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COLCHICINE IN ACUTE CORONARY SYNDROMES: A META-ANALYSIS OF 12.602 PATIENTS.","authors":"Luigi Cappannoli, Francesco Fracassi, Cristina Aurigemma, Enrico Romagnoli, Francesco Bianchini, Mattia Lunardi, Rocco Antonio Montone, Lazzaro Paraggio, Carlo Trani, Giovanna Liuzzo, Francesco Burzotta","doi":"10.1097/FJC.0000000000001706","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001706","url":null,"abstract":"<p><p>Inflammation is a leading cause of ischaemic heart disease. Aim of the present study is to assess whether treatment with colchicine in patients with ACS is associated with improved cardiovascular outcomes. We conducted a systematic review and meta-analysis of randomized clinical trials (RCTs) of patients with acute or recent ACS and treated with colchicine versus placebo. PubMed, Scopus, and the Cochrane Central Register of Controlled Trials databases were searched. The primary endpoint was composite of cardiovascular death, recurrent myocardial infarction (MI), stroke or urgent/unplanned revascularization. Other endpoints were individual components of the primary endpoint, all-cause death, non-cardiovascular death, and diarrhea. PROSPERO ID CRD42025648254. Three RCTs were included, involving 12,602 patients. There was no significant difference in the primary composite endpoint between the colchicine and placebo groups (OR 0.82, 95% CI 0.63-1.07, P=0.15). Analysis of individual components of the primary endpoint also revealed no significant differences between the colchicine vs. placebo groups: cardiovascular deaths (P=0.89), recurrent MI (P=0.17), strokes (P=0.27), urgent/unplanned revascularizations (P=0.14), all-cause death (P=0.95), non-cardiovascular death (P=0.98), and diarrhea (P=0.08). At the leave-one-out analysis, the exclusion of the CLEAR trial resulted in a significant reduction in primary endpoint (P=0.005). At further sensitivity analyses, the exclusion of patients who did not receive an initial twice-daily dose regimen and the exclusion of patients enrolled after COVID-19 pandemic resulted in a significant reduction in MACE (P=0.01 and P=0.001, respectively), reflecting heterogeneity among studies. The present meta-analysis raises new questions over the indication, timing and dosing of colchicine in patients with recent MI.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oltipraz ameliorates pressure overload-induced pathological cardiac hypertrophy in mice.","authors":"Junmou Hong, Huang Cao, Yan Wang","doi":"10.1097/FJC.0000000000001704","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001704","url":null,"abstract":"<p><p>Oltipraz (OPZ), a synthetic dithiothiol, is regarded as a novel agonist of nuclear factor erythroid-2 (Nrf-2). Recent studies revealed that Nrf-2 activation could suppress the pathological cardiac hypertrophy in mice. However, the therapeutic role of OPZ in the pathological cardiac hypertrophy remains incompletely understood. Thus, we evaluated the cardioprotective effects of OPZ in vivo and in vitro. Transverse aortic constriction (TAC) surgery was performed to induce the pathological cardiac hypertrophy in mice. In addition, the H9c2 cells were treated with angiotensin II (Ang II) to induce cardiomyocyte hypertrophy in vitro experiments. Our data revealed that OPZ relieved the TAC-induced pathological cardiac hypertrophy and myocardial damage in mice. Similarly, OPZ mitigated the increase in cardiomyocyte size induced by Ang II, indicating its ability to counteract cardiomyocyte hypertrophy. In addition, OPZ reduces cardiomyocyte oxidative stress, inflammation and apoptosis by activating Nrf-2 signaling in vivo and in vitro. Interestingly, our results also demonstrated that Nrf-2 knockdown abolished the protective effects of OPZ in vitro. Taken together, these data revealed that OPZ ameliorates the pathological cardiac hypertrophy via activating Nrf-2 signaling.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contemporary Analysis of cardiac Tamponade Etiologies, Treatments, and Outcomes: the CATEO Study.","authors":"Marco Giuseppe Del Buono, Mattia Brecciaroli, Gianluigi Saponara, Alessia D'Aiello, Daniela Pedicino, Gaetano Pinnacchio, Lorenzo Genuardi, Rocco Antonio Montone, Simone Filomia, Giulia La Vecchia, Ilaria Poli, Francesca Rigoli, Mariantonietta Di Salvatore, Michela Quirino, Jacopo Lenkowicz, Edoardo Pompei, Laura Antenucci, Giovanna Liuzzo, Carlo Trani, Giampaolo Tortora, Francesco Burzotta, Tommaso Sanna","doi":"10.1097/FJC.0000000000001702","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001702","url":null,"abstract":"<p><p>Cardiac tamponade is a critical condition resulting from various etiologies, including malignancies, inflammatory conditions and iatrogenic causes. With advances in treatments and changing epidemiology, there is a need to reassess the prevalence, management, and outcomes of pericardial tamponade. This study aimed to evaluate the current prevalence of different etiologies of tamponade, the management, and the clinical outcomes in a cohort of patients admitted to a high-volume Cardiac Intensive Care Unit (CICU). We conducted a retrospective analysis of 87 patients diagnosed with cardiac tamponade (median age 70 years; 51% male). Data on patient demographics, clinical characteristics, etiologies, treatment strategies, and outcomes were collected and analyzed. Malignant tamponade was the predominant etiology, observed in 47% of cases, with lung cancer being the most common. Other etiologies included inflammatory (22%), iatrogenic (20%), idiopathic (9%), and congestive heart failure-related (2%) effusions. The majority of patients (94%) underwent urgent percutaneous pericardiocentesis. Anti-inflammatory therapy was administered in 67% of cases, including NSAIDs (22%), colchicine (46%), steroids (24%) and IL-1 inhibitors (3%), with some patients receiving combination therapy. The 3-month all-cause mortality rate was 29%, with significantly higher mortality observed in patients with malignant effusions compared to non-malignant causes (49% vs. 11%, p<0.001). This study provides valuable insights into the clinical characteristics, management, and outcomes of patients with cardiac tamponade at a high-volume cancer center. Neoplastic pericardial effusion, particularly due to lung cancer, is the leading cause of tamponade in this cohort. Anti-inflammatory therapies were frequently used, but their role in improving outcomes requires further investigation. Mortality remains high, especially among those with malignancy-related effusions.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Muscarinic Acetylcholine Receptors in Oxytocin-Induced Cardioprotection Against Ischemia-Reperfusion Injury in Rats.","authors":"Mahdieh Faghihi, Mohammadreza Ahmadi-Beni, Fariba Houshmand","doi":"10.1097/FJC.0000000000001701","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001701","url":null,"abstract":"<p><p>Oxytocin (OT) has been shown to provide myocardial protection against ischemia-reperfusion (I/R) injury. This study investigates the involvement of muscarinic receptors in the OT-induced cardioprotection, focusing on its potential mechanisms and effects on myocardial infarction (MI) and ischemic arrhythmias. Male rats anesthetized with pentobarbital sodium were subjected to 25-min ischemia followed by 120-min reperfusion after intraperitoneal administration of OT (0.01 μg), atropine (1.5 µg/kg), or saline. Cardioprotection was evaluated by monitoring lactate dehydrogenase (LDH), malondialdehyde (MDA), and cardiac creatine kinase isoenzyme (CK-MB) levels, infarct size, arrhythmia severity, ventricular fibrillation, and mortality. OT markedly reduced infarct size, oxidative stress, and the severity of ischemic arrhythmias, including ventricular tachycardia and ventricular fibrillation, compared with saline-treated I/R animals. OT also significantly improved survival rates. Pretreatment with atropine abolished most protective effects of OT but did not significantly alter its suppression of ventricular fibrillation, suggesting the involvement of muscarinic receptor-independent mechanisms. These findings highlight that the OT-induced cardioprotection, mediated in part by acetylcholine (ACh) locally released in the left ventricle, extends beyond infarct limitation to include potent anti-arrhythmic effects. The dual impact of OT on MI and arrhythmias provides insights into the mechanisms underlying its preconditioning effect and its potential application in MI management.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aprocitentan for Treatment-Resistant Hypertension: Pharmacology Concepts and Clinical Insights.","authors":"Apryl N Peddi, Sarah E Wheeler, Keerthana Akkisetty, John D Bucheit","doi":"10.1097/FJC.0000000000001700","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001700","url":null,"abstract":"<p><p>Treatment resistant hypertension (TRH) occurs in nearly 20% of patients with a diagnosis of hypertension despite receiving three or more antihypertensives and places individuals at an increased risk of morbidity and mortality compared to essential hypertension. Numerous pathophysiological factors underlie TRH, including endothelin-1, which until recently no approved treatments targeted. Endothelin-1 exhibits multiple actions through binding to ETA and ETB receptors. Vasoconstriction of the vascular smooth muscle occurs when endothelin-1 binds ETA and ETB, however; vasodilation of endothelial cells also occurs through activation of ETB. Currently available endothelin receptor antagonists (ERA) were only approved for pulmonary hypertension until 2024 when the Food and Drug Administration approved aprocitentan as the first ERA for hypertension treatment in combination with other antihypertensives. The approval of aprocitentan occurred following the publication of the phase 3 PRECISION trial that compared aprocitentan versus placebo for patients with \"true\" TRH. Aprocitentan 12.5 mg exhibited a placebo-adjusted reduction in sitting systolic and diastolic blood pressure of 3.8/3.9 mmHg at 4 weeks of treatment. A dose-dependent increase in peripheral edema and a small reduction in hemoglobin due to hemodilution were greater in the aprocitentan-treated patients. Animal study data from past endothelin receptor antagonists showed this class of agents may lead to birth defects and was the basis for aprocitentan's black-box warning. Overall, clinical trial data supports aprocitentan's use as an effective agent for the TRH, but clinicians will need to individualize patient treatment selection and consider the safest and most efficacious options currently available.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Observation of the therapeutic effect of dapagliflozin on atherosclerosis in mice and preliminary exploration of the mechanism of action.","authors":"Fangfang Chen, Xu Wang, Yang Ma, Sihua Liu, Hongfei Sang","doi":"10.1097/FJC.0000000000001696","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001696","url":null,"abstract":"<p><p>In recent years, the incidence of Atherosclerosis (AS) has been increasing and has gradually become a major disease threatening human health. In this study, we analyzed the effect of dapagliflozin on AS and preliminarily explore the mechanism of action. First, apolipoprotein E (ApoE) knockout C57Bl/6J mice were used to establish an AS model in vitro. An intervention group treated with dapagliflozin and a model group treated with normal saline, both administered by gavage, were set up. The effects of dapagliflozin on macrophage polarization, blood lipids, inflammation, oxidative stress, and vascular adhesion of AS mice were observed, we found that compared with the model group, macrophages in the intervention group of mice were polarized from M2 to M1 type, the levels of inflammatory factors in the intervention group decreased, and the oxidative stress reaction and vascular adhesion were inhibited. Subsequently, the aorta tissues of mice were stained with HE and oil red O to observe their histopathological changes. We observed a significant improvement in aortic pathologic damage in the intervention group, converging to normal mice. Finally, autophagy in mouse aortic cells was determined, found the intervention group showed markedly increase Beclin-1 and LC3-II expression in the aorta than the model group. In conclusions, dapagliflozin can ameliorate the progression of AS, and its mechanism is related to the activation of aortic cell autophagy.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flavin adenine dinucleotide ameliorates pressure overload-induced heart failure by activating the short-chain acyl-CoA dehydrogenase.","authors":"Chunyu Chen, Xue Qin, Yuhong Cao, Liyuan Qing, Zhichao Ma, Qingping Xu, Huan Peng, Guifang Jin, Zhicheng Yang, Jieyu Xing, Sigui Zhou","doi":"10.1097/FJC.0000000000001698","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001698","url":null,"abstract":"<p><p>Flavin adenine dinucleotide (FAD), a cofactor that catalyzes the reaction of flavin protein, participates in fatty acid β-oxidation, which has been shown to inhibit pathological cardiac hypertrophy and fibrosis in spontaneously hypertensive rats. However, the therapeutic advantage of FAD for heart failure treatment has not been investigated. This study aimed to explore the effects and underlying mechanisms of FAD in a transverse aortic constriction (TAC)-induced heart failure mouse model and in vitro tert-Butyl hydroperoxide (tBHP)-induced cardiomyocyte apoptosis model experiments. FAD considerably inhibited tBHP-induced cardiomyocyte apoptosis. In addition, FAD significantly increased the activity and expression of the short-chain acyl-CoA dehydrogenase (SCAD) enzyme and ATP content while reducing the content of free fatty acids and reactive oxygen species both in vitro and in vivo. Meanwhile, FAD increased the mitochondrial membrane potential, suppressed mitochondrial membrane swelling, and decreased myocardial fibrosis and TUNEL-positive apoptosis cells in the TAC-induced heart failure mice. In conclusion, our results indicate that FAD plays a positive role in preventing and treating heart failure, which can be attributed in part to the activation of SCAD.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Factor XI as a Drug Target for the Prevention and Treatment of Thrombosis.","authors":"Nathaniel B Wayne, Sarah B Schaidle, Craig J Beavers","doi":"10.1097/FJC.0000000000001699","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001699","url":null,"abstract":"<p><p>The optimal anticoagulation therapeutic intervention balances preventing or treating thrombosis, depending on the clinical scenario, and bleeding. A novel drug target, factor eleven (FXI), may theoretically represent a way to prevent thrombosis in the clotting cascade, without increasing the risk of bleeding. Several mechanisms for inhibiting FXI or its activated form are being studied and include antisense oligonucleotides, monoclonal antibodies, small molecules, natural peptides, and aptamers. Many of the drugs that have been developed have been studied in clinical trials evaluating their use in secondary prevention of acute coronary syndromes, prevention of venous thromboembolism after orthopedic surgery, and stroke and systemic embolism prevention. Ongoing areas of interest include special patient populations such as patients with end stage renal disease (ESRD), cancer, and COVID-19 infection. FXI inhibition is a novel concept with many drug mechanisms that exist and are in varying stages of clinical study for a number of clinical uses.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}