Cardiovascular Toxicology最新文献

{"title":"QT Prolongation, Ventricular Arrhythmia, and Cardiac Arrest Signals During Ceftriaxone Co-therapy with Individual Proton Pump Inhibitors: A Multidatabase Study.","authors":"Yechao Chen, Qiaoling Gu, Mingnuo Zhao, Aijin Zhao, Zirui Kong, Haobin Shen, Yanan Zhang, Shuang Wang, Li Li, Han Xie, Peipei Liu, Haixia Zhang, Dayu Chen","doi":"10.1007/s12012-026-10174-z","DOIUrl":"10.1007/s12012-026-10174-z","url":null,"abstract":"<p><p>The concomitant use of ceftriaxone and proton pump inhibitors (PPIs) is common in hospital practice. However, it is unclear whether individual PPIs differ in their effects on QT interval prolongation, ventricular arrhythmia, or cardiac arrest, collectively termed as QVC events. We conducted a two-stage, real-world study. First, we screened the United States Food and Drug Administration Adverse Event Reporting System (FAERS) and the Canada Vigilance Adverse Reaction (CVAR) database with standard disproportionality measures (reporting odds ratio and proportional reporting ratio) and six drug-drug interaction (DDI) algorithms to identify combination signals that exceeded component signals. Second, we validated signal-positive combinations in the Medical Information Mart for Intensive Care IV (MIMIC-IV) intensive care unit (ICU) electronic health record (EHR) cohort by assembling adult inpatients with overlapping ceftriaxone-PPI exposures. The primary outcome was 28-day QVC events. Multivariable Cox proportional hazards models were the main analysis and complemented by propensity score matching, inverse probability of treatment weighting, and Fine-Gray competing-risk models. To address external generalisability, an additional validation was performed using ECG-ViEW II, an Asian electrocardiogram-linked real-world database. The combination of ceftriaxone and lansoprazole was significantly associated with QVC events, revealing notable DDIs (e.g., in FAERS, Ω025 = 0.54). To validate these findings, a cohort of 5,594 patients receiving ceftriaxone combined with PPIs from the MIMIC-IV database was analyzed using Cox proportional hazards models. The analyses corroborated the initial findings (lansoprazole vs. other PPIs, multivariate HR = 1.30; 95% CI: 1.10-1.54), with the risk associated with the three PPI combinations ranked as lansoprazole > pantoprazole > omeprazole. ECG-ViEW II provided supportive Asian external validation, showing a higher QVC risk for ceftriaxone plus lansoprazole than for ceftriaxone plus other PPIs. Evidence from two national pharmacovigilance systems and an ICU EHR cohort indicated that PPI choice modified cardiac safety during ceftriaxone therapy. Lansoprazole co-use confers a higher risk of QVC, whereas omeprazole appears relatively safer. Therefore, prospective confirmation is warranted.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13547183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900161","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":"Correction: Obesity Worsens Arsenic Trioxide-Induced Myocardial Toxicity and Its Protection by Metallothionein.","authors":"Tingwen Ge, Lei Qian, Aiwen Li, Qiang Guo, Qiuju Liu, Jiuwei Cui","doi":"10.1007/s12012-026-10182-z","DOIUrl":"10.1007/s12012-026-10182-z","url":null,"abstract":"","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886035","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":"Intravenous Exposure to Amino-polystyrene Induces Excessive Autophagy and Apoptosis in Myocardium Through ROS Driven PI3K/AKT/mTOR Axis.","authors":"Wen Gou, Yujun Xie, Rui Xia, Ping Gou, Chunfeng Cao, Fujun Luan, Beizhong Liu, Yuan Li","doi":"10.1007/s12012-026-10180-1","DOIUrl":"10.1007/s12012-026-10180-1","url":null,"abstract":"<p><p>Polystyrene (PS) is a pervasive plastic whose threat to human health is growing, yet its cardiotoxicity, particularly under clinically relevant exposure scenarios, remains poorly understood. This study addresses this critical gap by modeling intravenous exposure to nanopolystyrene, simulating clinical situations where plastic-derived medical devices directly contact blood. We established an in vitro model using human AC16 cardiomyocytes and an in vivo model via tail vein injection in Balb/c mice to compare the effects of amino-modified (PS-NH₂), carboxyl-modified (PS-COOH), and unmodified (PS-Bare) polystyrene nanoparticles. Our findings demonstrate that PS-NH₂, in contrast to PS-COOH and PS-Bare, induces significant cardiotoxicity. This toxicity was initiated by a substantial increase in reactive oxygen species (ROS), which subsequently suppressed the PI3K/AKT/mTOR signaling axis. This inhibition led to the excessive activation of autophagy and the induction of apoptosis in cardiomyocytes. In vivo, PS-NH₂ exposure caused severe pathological changes in mouse hearts, confirming its potent cardiotoxicity, characterized by inflammation, an impaired oxidative-antioxidant balance, and adverse cardiac remodeling. Notably, these detrimental effects were substantially reversed by the ROS scavenger N-acetylcysteine (NAC) or ginsenoside Rb1. In conclusion, our study reveals that Polystyrene positively charged amino-modified during degradation is the key to its cardiotoxicity, operating through a ROS-driven PI3K/AKT/mTOR pathway. These findings underscore the potential risks associated with specific surface modifications of nanoplastics and provide crucial insights for developing therapeutic strategies against plastic-induced cardiac injury.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13529858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863662","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":"Toxic Metal-Essential Trace Element Imbalance in Cardiometabolic Disease: Ferroptosis as a Mechanistic Link Between Environmental Exposure and Vascular Injury.","authors":"Ahmed Farid Gadelmawla, Sara Hosny El-Farargy, Amal A Alsubaiei, Najat Y AlSejari, Mahmoud Hekal, Hamza A Abdul-Hafez, Ahmed Elmorsy Mohamed, Ahmed W Hageen, Abdullah M Alharran, Giuseppe Andò, Wilbert S Aronow","doi":"10.1007/s12012-026-10178-9","DOIUrl":"10.1007/s12012-026-10178-9","url":null,"abstract":"<p><p>Cardiometabolic diseases, including cardiovascular disease, type 2 diabetes mellitus (T2DM), obesity-related metabolic dysfunction, and hypertension, remain major causes of global morbidity and mortality. Beyond traditional risk factors, environmental exposure to toxic metals is increasingly recognized as a contributor to vascular and metabolic injury. Lead, cadmium, arsenic, and mercury are persistent toxicants that may accumulate in human tissues and interfere with essential trace-element homeostasis. This narrative review examines how toxic metal exposure disrupts the biological balance of iron, zinc, copper, and selenium, thereby weakening mitochondrial function, antioxidant defense, endothelial regulation, and metabolic stability. A central focus is ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation and failure of protective systems such as the selenium-GPX4-glutathione axis. Toxic metal-essential trace-element imbalance may create a pro-ferroptotic environment that promotes endothelial dysfunction, nitric oxide impairment, vascular stiffness, atherosclerotic plaque instability, myocardial ischemic vulnerability, insulin resistance, β-cell dysfunction, and cardiometabolic clustering. This review reframes heavy metal-associated cardiometabolic disease as a consequence of toxic metal-essential trace-element dyshomeostasis rather than direct toxicity alone. Clinically, this framework supports targeted exposure history, careful interpretation of metal and trace-element biomarkers, correction of documented deficiencies, and avoidance of indiscriminate supplementation. Future studies integrating exposomics, metallomics, ferroptosis biomarkers, and longitudinal cardiometabolic outcomes are needed to clarify causality and guide prevention.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863702","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":"Hypoxia-Driven Mechanisms in Ischemic Heart Failure: A Bioinformatics, Machine Learning and Bayesian Network Study.","authors":"Quancheng Han, Ruiqi Fan, Jingjing Ma, Huajing Yuan, Yonghong Guo, Yitao Xue, Yiding Yu, Yan Li","doi":"10.1007/s12012-026-10177-w","DOIUrl":"10.1007/s12012-026-10177-w","url":null,"abstract":"<p><p>Hypoxia is a critical determinant in the etiology and progression of ischemic heart failure, but its underlying molecular mechanisms and regulatory interactions remain largely enigmatic. in our study, we employed differential analysis, coupled with WGCNA and the MSigDB database, to identify nine genes associated with hypoxia in heart failure. GO and KEGG enrichment analyses indicated that these genes are predominantly involved in hypoxia, immune responses, inflammation, apoptosis, and aging processes.Employing Bayesian networks, we elucidated four regulatory relationships among the hypoxia genes: PIM1-CDKN1A, IL6-CDKN1A, PLIN2-ANGPTL4, and SERPINE1-PLAUR. We amalgamated 12 machine learning algorithms, comprising 113 distinct combinations, to refine our findings and identified four pivotal hypoxia genes: SLC2A1, PLIN2, FOSL2, and PIM1. The SHAP analysis was instrumental in interpreting the predictive outcomes of the optimal model, the Random Forest algorithm, SLC2A1 was the most influential gene in the model. Immune infiltration analysis revealed the presence of seven types of dysregulated immune cells within the failing myocardium. Colocalization analysis showed that the posterior probabilities were predominantly concentrated on the gene-expression-only hypothesis and did not provide sufficient evidence for shared causal variants between the candidate-gene eQTL and HF GWAS signals. Overall, our research offers significant insights into the molecular mechanisms of hypoxia genes in the pathophysiology of heart failure, paving the way for the development of targeted and immunomodulatory therapies.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825498","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":"Integrated Multi-omics Reveals CDKN1A Suppression and Metabolic Regulation as Key Mechanisms of Huangqi Guizhi Wuwu Decoction Against Doxorubicin-Induced Cardiotoxicity.","authors":"Qian Hou, Xinyue Yu, Ke Wu, Siling Chen, Xin Mao, Xinying Qian, Changjin Li, Lidan Sheng, Ruiping Wang, Yin Huang","doi":"10.1007/s12012-026-10168-x","DOIUrl":"10.1007/s12012-026-10168-x","url":null,"abstract":"<p><p>The clinical utility of doxorubicin (DOX) is severely limited by dose-dependent cardiotoxicity, for which effective interventions remain scarce. Huangqi Guizhi Wuwu Decoction (HGWD) shows promising cardioprotective potential, but its mechanisms against DOX-induced cardiotoxicity (DIC) remain unexplored. This study explored the molecular mechanisms using an integrated metabolomics and transcriptomics approach. We identified 57 compounds in HGWD by liquid chromatography ion trap time-of-flight mass spectrometry (LC-IT-TOF/MS), and quantified five representative compounds for standardization. Mice were randomized into six groups: control, DOX (10 mg/kg × 2), DOX + low-dose HGWD (7 g/kg/d), DOX + high-dose HGWD (14 g/kg/d), DOX + dexrazoxane (100 mg/kg × 2), and HGWD (14 g/kg/d) alone. HGWD effectively alleviated cardiac dysfunction and reduced serum injury markers, with the high-dose group demonstrating efficacy comparable to the positive control drug, dexrazoxane. Subsequently, multi-omics profiling was performed on heart tissues from the control, DOX, and DOX + high-dose HGWD groups. Metabolomics identified 31 differential metabolites, highlighting energy metabolism restoration (e.g., acylcarnitines, citric acid) and inflammatory mediator modulation (e.g., arachidonic acid). Transcriptomics uncovered 37 genes enriched in innate immunity (e.g., Irf7, Isg15) and apoptosis (e.g., Bax, Cdkn1a). Network analysis constructed a core regulatory module, pinpointing CDKN1A as a potential mediator. Validation experiments confirmed that HGWD suppressed DOX-induced CDKN1A upregulation in mouse hearts. Furthermore, in H9c2 cells, HGWD mitigated DOX-induced apoptosis and inflammation, exhibiting cytoprotection comparable to pifithrin-α, a specific p53 inhibitor. In summary, HGWD protects against DIC by modulating a multi-target network and the suppression of CDKN1A represents a key underlying mechanism.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788435","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":"Cardio-Oncology in Cold Climates: Epidemiological Features, Bidirectional Interaction Mechanisms, and Integrated Management Strategies.","authors":"Yuexin Li, Yifei Zhang, Haobo Sun, Ying He, Dongqing Gao, Tingting Ding, Xuemei Chen, Zhonghua Sun, Shuai Jiang, Mei Dong","doi":"10.1007/s12012-026-10175-y","DOIUrl":"10.1007/s12012-026-10175-y","url":null,"abstract":"<p><p>Cardiovascular disease (CVD) and cancer are leading causes of death worldwide, with their comorbidity posing a major public health challenge. In cold regions (latitude ≥ 45° or annual mean temperature ≤ 10 °C), this dual burden is exacerbated by unique environmental exposures and lifestyle factors. This review aims to systematically characterize the epidemiological features of CVD and cancer in cold regions, elucidate the mechanisms by which cold exposure synergistically exacerbates cancer therapy-related cardiovascular toxicity (CTR-CVT), and propose a comprehensive, cold-region-tailored management framework for the prevention, treatment, and rehabilitation of cardio-oncology comorbidity. Cold regions show significantly higher age-standardized incidence and mortality rates for both CVD and cancer compared to temperate regions. Low temperatures, high-sodium diets, and air pollution synergistically increase cardiovascular risk, while lung, colorectal, breast, and prostate cancers substantially exceed global averages. The bidirectional interaction between CVD and cancer involves multiple mechanisms. Cancer therapies induce cardiotoxicity via oxidative stress, mitochondrial dysfunction, ferroptosis, and inflammatory pathways. Conversely, CVD promotes cancer progression through chronic inflammation, neurohormonal activation, cardiac-derived factors, and exosome-mediated communication. Cold stress, acting as a synergistic toxicological factor, exacerbates comorbidity through sympathetic overactivation, amplification of oxidative and inflammatory cascades, and metabolic remodeling that disrupts drug metabolism and myocardial energy supply. In conclusion, CVD-cancer comorbidity in cold regions represents a distinct entity shaped by environmental and lifestyle factors. We propose a full-cycle, cold-region-tailored management system including cold adaptation training, dietary modification, vitamin D supplementation, integrated traditional Chinese and Western medicine, and dynamic monitoring of cardiometabolic and tumor markers. Future research should prioritize large-scale prospective studies, multi-omics approaches for sensitive biomarker identification, and region-specific interventions to reduce this dual disease burden.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788521","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":"Metallomic Dysregulation and Cardiovascular Disease: Essential Trace Elements, Non-essential Metal Exposure, and Heart Failure Risk: A Systematic Review.","authors":"Abiya Ahad, Darshan Hullon","doi":"10.1007/s12012-026-10172-1","DOIUrl":"10.1007/s12012-026-10172-1","url":null,"abstract":"<p><p>Heart failure (HF) affects over 64 million people worldwide, with five-year mortality rates rivaling solid-organ malignancies. Despite advances in neurohormonal therapy, many patients continue to progress, suggesting additional pathophysiological drivers. Metallomic dysregulation-imbalance among essential trace elements combined with non-essential metal accumulation-engages pathways central to HF pathobiology, including oxidative stress, mitochondrial dysfunction, impaired calcium handling, and pro-fibrotic cascades. We conducted a systematic review compliant with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement, searching PubMed/MEDLINE, Embase, Scopus, and Web of Science. Eligible studies enrolled adults who were assessed for at least one metal and reported a cardiac outcome. Risk of bias was evaluated using the Cochrane risk-of-bias tool for randomized trials (RoB 2) and the Newcastle-Ottawa Scale. Twenty-nine studies met the inclusion criteria-encompassing over 90,000 participants. Iron deficiency affected approximately 30-58% of patients with HF. In HF with reduced ejection fraction (HFrEF), intravenous ferric carboxymaltose improved Patient Global Assessment (odds ratio [OR] 2.51; 95% confidence interval [CI] 1.75-3.61) and reduced HF hospitalization (hazard ratio [HR] 0.39; 95% CI 0.19-0.82). Zinc, selenium, and magnesium deficiencies were associated with impaired antioxidant defenses, mitochondrial dysfunction, and susceptibility to arrhythmias. Among non-essential metals, cadmium showed the strongest prospective evidence for adverse cardiovascular outcomes, including HF risk and cardiac remodeling. Lead was associated with left ventricular hypertrophy and cardiovascular mortality, while arsenic was consistently linked to cardiovascular mortality. Evidence for mercury remained limited and inconsistent. Intravenous (IV) iron repletion in iron-deficient HFrEF is the only metallomic intervention with robust evidence. Remaining associations are hypothesis-generating. Adequately powered trials and Mendelian randomization studies are urgently needed. Registration number: PROSPERO CRD420261343598.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788514","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":"Senolytics Reverse PM_2.5 - Induced Cell and Vascular Dysfunction.","authors":"Daniel Gomes, Samantha A McFall, Ning Chen, Jingjing Zhao, Sanjay Srivastava, Daniel J Conklin, Timothy E O'Toole","doi":"10.1007/s12012-026-10171-2","DOIUrl":"10.1007/s12012-026-10171-2","url":null,"abstract":"<p><p>Exposure to fine airborne particulate matter (PM_2.5) is associated with cardiovascular disease and increased atherogenesis. While some prior studies provided mechanistic insights linking exposure to lesion progression, instability, and rupture, a complete definition of cellular events contributing to early vascular inflammation is lacking. Here we show that C57BL/6J mice exposed to concentrated ambient PM_2.5 (CAP), as opposed to control mice inhaling filtered air, displayed endothelial activation, as evidenced by the increased number of leukocytes rolling on, and adhering to, the intact vasculature in vivo. As CAP exposure also induced the senescence of peripheral blood mononuclear cells (MNCs) and endothelial progenitor cells (EPCs), we further assessed the role of this outcome in PM_2.5-induced vascular dysfunction. We observed that treatment with the senolytics Dasatinib and Quercetin (DQ), which eliminate senescent cells, was effective in reversing the CAP-induced senescence of both of MNCs and EPCs as demonstrated by reductions in β-galactosidase activity and the expression of genes characteristic of the senescence activated secretory phenotype (SASP). Furthermore, we found that DQ treatment was effective in reversing CAP-induced defects in in vitro EPC function (tube forming capacity) and limited in vivo endothelial activation as well. These results provide strong evidence for a role of PM_2.5 in the early stages of atherogenesis by inducing endothelial activation leading to leukocyte recruitment. Our results further suggest that senolytic treatment may be efficacious in combatting adverse cardiovascular outcomes in those chronically exposed to high levels of PM_2.5.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13473078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148721063","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":"Correction: Evaluation of Electrocardiogram Parameters and Heart Rate Variability During Blood Pressure Elevation by Phenylephrine in Cirrhotic Rats.","authors":"Farzaneh Ketabchi, Mohammadreza Khoram, Amirreza Dehghanian","doi":"10.1007/s12012-026-10162-3","DOIUrl":"10.1007/s12012-026-10162-3","url":null,"abstract":"","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":"26 8","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705575","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}