Cardiovascular Toxicology心血管毒理学
Cardiovascular Toxicology(英文缩写 CARDIOVASC TOXICOL),ISSN 1530-7905,eISSN 1559-0259,中文译名:心血管毒理学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 2.755 | Q3 |
| 2022 | 3.200 | Q2 |
| 2023 | 3.400 | Q2 |
| 2024 | 3.700 | Q1 |
| 2025 | 3.300 | Q2 |
Cardiovascular Toxicology 最新收录文献
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1. The Interplay Between Thyroid Cancer and Cardiovascular Disease: Shared Mechanisms, Treatment Implications, and Survivorship Perspectives.
PMID:日期:2026-09-21The global incidence of thyroid cancer (TC), particularly differentiated thyroid cancer (DTC), has increased substantially over recent decades, while cardiovascular disease (CVD) remains the leading cause of death globally. As advances in diagnosis and treatment have significantly improved long-term survival in thyroid cancer patients, attention has increasingly shifted toward non-cancer complications, especially cardiovascular morbidity and mortality. Current evidence indicates that TC survivors have a higher risk of atrial fibrillation (AF), coronary artery disease (CAD), stroke, heart failure, and other cardiovascular complications than the general population. This association appears to result from a complex interaction between shared cardiometabolic risk factors and biological pathways. Obesity, metabolic syndrome, diabetes, hypertension, and dyslipidemia promote chronic inflammation, endothelial dysfunction, and insulin/IGF signaling, which contribute to atherosclerosis and tumor progression. Thyroid hormone dysregulation provides an additional link between thyroid cancer management and cardiovascular risk. Long-term thyroid-stimulating hormone (TSH) suppression therapy may induce subclinical hyperthyroidism and increase susceptibility to atrial fibrillation, ischemic heart disease, cardiac remodeling, and vascular dysfunction. Treatment-related factors, including thyroidectomy, radioactive iodine therapy, and targeted therapies, may also contribute to cardiovascular toxicity and influence long-term cardiovascular outcomes. Importantly, cardiovascular risk is heterogeneous among thyroid cancer survivors and may vary according to thyroid cancer risk category and current disease status, the intensity and duration of TSH suppression, radioactive iodine exposure, and patient-level characteristics such as age, sex, and baseline cardiovascular risk. This review synthesizes epidemiological and mechanistic evidence linking TC and CVD, with particular emphasis on shared metabolic and inflammatory pathways, hormonal and treatment-related factors, and changes in cardiovascular risk across different phases of thyroid cancer survivorship. Recognizing these determinants may support individualized cardiovascular risk assessment and help balance the oncologic benefits of thyroid cancer treatment against its potential long-term cardiovascular consequences.
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2. The Potential Role of the Gut-Vascular Axis in Ciprofloxacin-Associated Aggravation of Aortic Dissection.
PMID:日期:2026-09-21Ciprofloxacin (CIP) is associated with an increased risk of aortic dissection (AD); however, the underlying mechanism remains unclear. This study investigates the potential contribution of gut microbiota and intestinal barrier alterations to CIP-associated AD progression. The AD model was established using a combination of β-aminopropionitrile and angiotensin II. The composition of the gut microbiota was analyzed using 16 S rRNA sequencing. In vivo experiments were conducted to investigate whether CIP aggravates AD through a potential gut-vascular axis involving intestinal alterations and increased circulating lipopolysaccharide (LPS) levels, which was further explored in human aortic smooth muscle cells (HASMCs). The results showed that CIP aggravated aortic injury and induced smooth muscle cell dysfunction in AD mice. CIP disrupted gut microbial composition and impaired intestinal barrier integrity, which was accompanied by increased circulating LPS levels. Additionally, in vitro experiments demonstrated that combined CIP and LPS stimulation enhanced HASMC apoptosis and phenotypic switching. Our findings suggest that CIP-associated intestinal alterations and elevated circulating LPS levels may contribute to AD progression through a potential gut-vascular axis, providing new insights into fluoroquinolone-associated vascular injury and potential gut-targeted interventions.
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3. Association Between Blood Heavy Metals and Selenium with All-Cause Mortality in Cardiovascular-Kidney-Metabolic Syndrome Populations: Exploring the Mediating Effects of Inflammatory Biomarkers.
PMID:日期:2026-09-21Cardiovascular-kidney-metabolic (CKM) syndrome, characterized by the pathophysiological interplay among metabolic disorders, chronic kidney disease (CKD), and cardiovascular disease (CVD), significantly elevates mortality risk. Environmental heavy metal exposure and selenium deficiency are implicated in these conditions, but their combined impact on CKM syndrome is unclear. To investigate the associations of blood heavy metals (lead [Pb], cadmium [Cd], mercury [Hg], manganese [Mn]) and selenium (Se) with all-cause mortality in CKM populations, and examine the mediating role of inflammatory biomarkers. This cross-sectional study with prospective mortality follow-up included 6,072 participants from NHANES (2011-2018). Kaplan-Meier curves, multivariable Cox regression models, and restricted cubic spline (RCS) analyses were employed to assess all-cause mortality associations. Subgroup and interaction analyses evaluated risks across demographic strata. Mediation analysis was employed to explore the mediating effects of inflammatory biomarkers (NLR, MLR, NMLR, and SIRI). The Weighted quantile sum (WQS) model was utilized to estimate the effects of combined blood metal exposures. Among 6,072 participants, 409 deaths occurred during follow-up. In the fully adjusted model, there was a significant negative correlation between blood selenium levels and all-cause mortality in the CKM population. Compared with the lowest quartile (Q1), the highest selenium quartile (Q4) was associated with a 38% reduced mortality risk (HR = 0.62, 95% CI: 0.45-0.85, P = 0.003). RCS analysis revealed an L-shaped dose-response relationship (P for nonlinear = 0.002). Subgroup analyses confirmed consistent associations in both non-advanced CKM (stages 0-2) and advanced CKM (stages 3-4) (all P < 0.05, P for interaction = 0.163). Mediation analysis revealed that NLR, MLR, NMLR, and SIRI partially mediated the association between blood selenium and all-cause mortality, and the mediated proportions were relatively modest (ranging from 3.57 to 5.29%). Higher blood selenium was associated with reduced all-cause mortality in CKM syndrome after adjustment for measured confounders, and mediation analysis suggested a potential partial role of inflammation in this association. These findings underscore the need for targeted interventions to mitigate mortality in this high-risk population.
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4. Genetic and Molecular Determinants of Cancer Therapy-Related Cardiovascular Toxicity.
PMID:日期:2026-09-20Cancer therapy-related cardiovascular toxicity (CTR-CVT) is an umbrella term for myocardial, vascular, electrical, and inflammatory complications of cytotoxic, targeted, immune, and radiation-based therapies. Cancer therapy-related cardiac dysfunction (CTRCD) is used here more narrowly for treatment-related myocardial dysfunction, typically identified by changes in left ventricular ejection fraction, global longitudinal strain, and/or cardiac biomarkers. The pathophysiology of CTR-CVT is multifactorial, but the implicated pathways should not be interpreted as equally causal. The dominant initiating mechanism is therapy-specific - anthracycline injury is best supported by topoisomerase IIβ (TOP2B)-mediated DNA damage with secondary mitochondrial and redox injury; HER2-directed toxicity by disruption of NRG1-ERBB2/ERBB4 survival signalling; fluoropyrimidine toxicity by coronary vasomotor dysfunction; VEGF-pathway inhibition by endothelial dysfunction and hypertension; immune checkpoint inhibitor toxicity by loss of immune tolerance; and radiotherapy injury by endothelial and microvascular damage with progressive fibrosis. Mitochondrial dysfunction, oxidative stress, inflammation, calcium dysregulation, apoptosis, and ferroptosis frequently act as downstream or amplifying pathways, although the clinical relevance of several regulated cell-death mechanisms remains incompletely established. Genetic susceptibility may further modify risk, but the strength of evidence differs among reported loci. Replicated pharmacogenetic associations, rare variants in established cardiomyopathy genes, and preliminary candidate-gene findings should therefore be considered separately. Most available studies remain limited by small cohorts, heterogeneous phenotyping, ancestry imbalance, and incomplete external replication. This review critically evaluates the hierarchy and strength of mechanistic and genetic evidence and discusses the extent to which these findings can currently inform risk stratification, surveillance, prevention, and treatment in precision cardio-oncology.
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5. Exposure to Polystyrene Nanoplastics Induces Ferroptosis-Associated Cardiac Injury: Cell-Based Evidence for Lysosome-Associated NLRX1 Loss and an NLRX1-STING-NCOA4 Response.
PMID:日期:2026-09-19Nanoplastics are widespread environmental contaminants encountered through ingestion and inhalation, raising concerns about their cardiovascular toxicity. How polystyrene nanoplastics (PS-NPs) disrupt cardiomyocyte iron homeostasis remains unclear. We hypothesized that reduced NLR family member X1 (NLRX1) links PS-NP exposure to stimulator of interferon genes (STING) signaling and nuclear receptor coactivator 4 (NCOA4)-associated iron dysregulation. We examined primary neonatal mouse ventricular cardiomyocytes and an 8-week oral-exposure mouse model. In both models, PS-NPs reduced NLRX1 and glutathione peroxidase 4 (GPX4) protein levels, increased STING phosphorylation and acyl-CoA synthetase long-chain family member 4 (ACSL4) expression, and promoted iron accumulation and lipid peroxidation. Cell viability declined, and mice developed cardiac dysfunction and fibrosis. In cardiomyocytes, NLRX1 mRNA remained unchanged. Bafilomycin A1 attenuated NLRX1 protein loss, while NLRX1 showed greater spatial association with lysosome-associated membrane protein 1 (LAMP1)-positive compartments. NLRX1 overexpression reduced STING phosphorylation, iron accumulation, and lipid peroxidation. STING silencing decreased NCOA4 and increased ferritin heavy chain 1, whereas NCOA4 silencing attenuated GPX4 downregulation and ACSL4 upregulation. Re-expression experiments supported the functional ordering of NLRX1, STING, and NCOA4. Ferrostatin-1 (Fer-1) co-treatment attenuated iron accumulation, lipid peroxidation, and GPX4/ACSL4 changes in both models. It improved cardiomyocyte viability and attenuated cardiac dysfunction and fibrosis, although the myocardial phosphorylated-to-total STING ratio remained above control levels. These findings support ferroptosis-associated cardiac injury following PS-NP exposure, with cellular evidence implicating lysosome-associated NLRX1 protein loss and a downstream STING-NCOA4 response.
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6. The Effect of Serum Trace Element Levels On Cardiovascular Diseases in Adults in the Ravansar Region (Western Iran): A Risk Assessment Study in the Context of Elevated Lipid Profiles.
PMID:日期:2026-09-17Cardiovascular diseases (CVDs) are acknowledged as a primary contributor to global human mortality, including in Iran. There is growing interest in understanding the interactions between toxic and essential elements in the body. Therefore, the objective of this research was to examine how levels of essential and toxic elements affect the risk of cardiovascular disease among individuals with elevated serum lipid levels. This case-control study was conducted using data from the Kurdish population participating in the Ravansar Non-Communicable Diseases (RaNCD) study in the Ravansar region of western Iran. Samples were received from the Ravansar Cohort Biobank between August 2023 and December 2023. A total of 300 participants were recruited, comprising 150 individuals with cardiovascular diseases (CVDs) as cases and 150 controls. Blood concentrations of total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) were measured in all participants. Serum levels of arsenic (As), mercury (Hg), nickel (Ni), cadmium (Cd), lead (Pb), zinc (Zn), copper (Cu), chromium (Cr), and iron (Fe) were determined using inductively coupled plasma mass spectrometry (ICP-MS). Logistic regression models were used to assess the risk of CVD by comparing the second, third, and fourth quartiles of elemental concentrations with the first quartile. The results of current study showed that CVDs patients were older (mean age: 52.8 yrs vs. 45.8 yrs), less educated (65.3% vs. 44% illiterate), and mostly living in rural areas. CVDs patients with elevated levels of TC, TG, and LDL/HDL ratio had higher levels of As but lower levels of Cr as compared to controls. The levels of essential elements were comparable between the two groups. In single-metal models adjusted for potential confounders, higher quartiles of As, Ni, Fe, and Hg were associated with an increased risk of CVD among individuals with elevated TC, TG, or LDL/HDL ratio levels. However, after simultaneous adjustment for all measured metals (Model 2 with Firth correction), only As and Ni remained independently associated with elevated risk. For instance, among participants with elevated TC, the odds ratios (ORs) for CVD associated with As exposure were 7.05 (95% CI: 3.19-16.3; p < 0.001), 3.54 (95% CI: 1.65-7.83; p = 0.001), and 3.33 (95% CI: 1.55-7.37; p = 0.002) for the second, third, and fourth quartiles, respectively, compared with the reference quartile. Elevated Ni levels were also associated with an increased risk of CVD for third (15.6; 95% CI: 6.59-40.3; p < 0.001) and fourth quartile (2.83; 95% CI: 1.30-6.35; p = 0.001). The associations for Hg and Fe were attenuated and no longer statistically significant in the fully adjusted models. Conversely, higher Zn and Cr levels were associated with reduced CVD risk, with ORs below 1.0 and 95% confidence intervals that did not include 1.0. Higher blood levels of As and Ni were independently associated with an increased risk of CVD, whereas higher Cr and Zn levels were associated with a reduced risk. Although mercury and iron showed associations in single-metal models, these did not persist after adjustment for co-exposure to other metals and thus were not identified as independent risk factors in this population. These findings suggest that both toxic and essential elements may play important roles in cardiovascular health, particularly among individuals with dyslipidemia, and highlight the importance of considering mixed-metal exposures when evaluating cardiovascular risk.
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8. Revealing the Link Between Exposure to Per- and Polyfluoroalkyl Substances (PFAS) and Stroke: A Comprehensive Epidemiological and Network Toxicology Perspective.
PMID:日期:2026-09-13Per- and polyfluoroalkyl substances (PFAS) are persistent environmental pollutants associated with cardiovascular disease; however, their association with stroke risk remains insufficiently characterized. Critical knowledge gaps remain regarding the dose-response relationships, mixture effects, and biological pathways potentially linking PFAS to cerebrovascular disease. We initially screened 50,912 U.S. adults from NHANES (2003-2012) and included eligible participants to examine associations between serum PFAS concentrations, including PFOA, PFOS, PFHxS, and PFNA, and self-reported stroke. Weighted generalized linear models assessed exposure-response relationships and weighted quantile sum (WQS) regression were used to evaluate PFAS mixture effects. Causal mediation analysis quantified the contributions of serum lipids (total cholesterol [TC] and LDL-cholesterol) to the PFAS-stroke associations. Individual PFAS showed positive associations with stroke. Near-linear dose-response curves suggested no apparent thresholds for PFOA, PFHxS, and PFNA (all P for trend < 0.01), while PFOS exhibited a threshold effect at 3.73 ng/mL (95% CI: 3.15-4.28). WQS regression indicated that PFAS mixtures were positively associated with stroke risk (OR = 1.52; 95% CI: 1.17-1.97), with PFOS contributing the largest mixture weight (0.39). Mediation analyses indicated TC and LDL mediated 2.07-11.22% of the PFAS-stroke associations (P mediation < 0.05). This study establishes PFAS exposure, particularly PFOS-dominated mixtures, may represent an environmental correlate of stroke risk, with lipid dysregulation potentially contributing to this association. Strategies aimed at reducing PFOS exposure may help mitigate the potential cerebrovascular burden associated with PFAS exposure.
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9. Phthalate and Terephthalate Mixtures, Cardiometabolic Risk Factors, and the Role of Oxidative Stress: Evidence from NHANES 2015-2018.
9. 邻苯二甲酸酯和对苯二甲酸酯混合物、心脏代谢危险因素和氧化应激的作用：来自NHANES 2015-2018的证据PMID:日期:2026-09-11Phthalates are a class of endocrine-disrupting chemicals that may impair glucose and lipid metabolism through oxidative stress pathways. In this study, we analyzed NHANES 2015-2018 data on 2,336 U.S. adults and assessed fifteen phthalate and terephthalate metabolites, four glycemic outcomes, and five lipid outcomes. We used multivariable weighted quantile sum (WQS) regression to examine negative and positive associations of phthalate/terephthalate mixtures with glycemic and lipid outcomes. We assessed mediation by oxidative stress via gamma-glutamyltransferase (GGT) and explored modification by a composite score of dietary and lifestyle anti- and pro-oxidants (i.e., oxidative balance score, OBS) through the inclusion of product terms (WQS index*OBS) in linear regressions. A one-decile increase in phthalate/terephthalate mixtures dominated by mono(2-ethyl-5-hydroxyhexyl) terephthalate was associated (Estimate; 95% CI) with higher fasting glucose (1.95; 0.75, 3.14), fasting insulin (9.10%; 6.32%, 11.95%), HOMA-IR (9.86%; 6.86%, 12.94%), and HbA1c (0.05; 0.03, 0.07). Phthalate/terephthalate mixtures were associated with lower HDL-C (-0.93; -1.26, -0.60), LDL-C (-2.28; -3.54, -1.02), and total cholesterol (TC) (-1.89; -2.86, -0.93), and with higher fasting triglycerides (2.98%; 0.77%, 5.23%). GGT mediated a limited number of associations. OBS attenuated adverse associations between phthalate/terephthalate mixtures and select lipid outcomes, including HDL-C and TC/HDL-C ratio, among females. Overall, exposure to a mixture of phthalate/terephthalate metabolites was associated with disrupted glucose and lipid metabolism markers in this cross-sectional study. Oxidative stress may play a role in some of these associations, potentially providing a target for intervention, but longitudinal and randomized trials are needed to confirm these findings.
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10. Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.
PMID:日期:2026-09-11Myocardial injury is a common pathological endpoint in conditions such as acute myocardial infarction, ischemia/reperfusion injury, myocarditis, and drug-induced cardiotoxicity, and remains a therapeutic challenge due to the irreversible loss of cardiomyocytes and subsequent ventricular remodeling. Current strategies lack effective interventions directly targeting regulated cell death pathways. This review centers on the dysregulation of the regulated cell death (RCD) and autophagic network. We comprehensively integrate the dual roles, and evidence-graded crosstalk among RCD modalities (apoptosis, pyroptosis, and ferroptosis) and autophagic responses, proposing a paradigm shift from isolated pathway inhibition to dynamic rebalancing of the RCD and autophagic network for cardioprotection. Within this framework, we consolidate and compare evidence illustrating how active metabolites, single botanical drugs, and compound formulations of traditional Chinese medicine regulate multiple forms of RCD-associated signaling and autophagic processes. The multi-metabolite, multi-target nature enables coordinated regulation at the cellular survival-death checkpoint. Mechanistically, TCM interventions can: (1) attenuate apoptotic marker expression and context-dependently modulate autophagic responses via axes such as PI3K/Akt/mTOR, AMPK/mTOR, MAPK, and JAK/STAT; (2) suppress NLRP3/caspase-1/GSDMD-mediated pyroptotic signaling markers; and (3) modulate lipid peroxidation-associated ferroptotic signaling through antioxidant pathways centered on the Nrf2/GPX4 and System x axes. These actions collectively ameliorate upstream pathological loops involving oxidative stress, inflammatory amplification, and mitochondrial dysfunction. This review adopts a comprehensive cardiovascular toxicology perspective to integrate the regulatory mechanisms of RCD and autophagic networks in myocardial injury, encompassing both exogenous drug-induced cardiotoxicity (e.g., doxorubicin) and endogenous toxic stresses, including lipotoxicity, ROS-mediated toxicity, and ischemia-related metabolic injury. Notably, many TCM agents exhibit cross-RCD and autophagic synergistic effects supported by direct perturbation-and-rescue evidence (Level c crosstalk) as well as co-regulatory profiles, suggesting that cardioprotection at the network level may be achieved through shared hub nodes. This perspective provides a clearer mechanistic landscape for elucidating the action of TCM formulas and for screening novel therapeutic candidates. Ultimately, it advocates for advancing traditional Chinese medicine-based myocardial protection strategies into reproducible, quantifiable, and clinically verifiable pharmacological research systems oriented around RCD and autophagic network homeostasis.