Cardiovascular Toxicology最新文献_第3页

ETV5-Mediated Transcriptional Repression of DDIT4 Blocks Macrophage Pro-Inflammatory Activation in Diabetic Atherosclerosis. ETV5 介导的 DDIT4 转录抑制阻断了糖尿病动脉粥样硬化中巨噬细胞的促炎症激活。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-26 DOI: 10.1007/s12012-024-09956-0

Lili Shi, Tingting Sun, Di Huo, Lin Geng, Chao Zhao, Wenbo Xia

{"title":"ETV5-Mediated Transcriptional Repression of DDIT4 Blocks Macrophage Pro-Inflammatory Activation in Diabetic Atherosclerosis.","authors":"Lili Shi, Tingting Sun, Di Huo, Lin Geng, Chao Zhao, Wenbo Xia","doi":"10.1007/s12012-024-09956-0","DOIUrl":"https://doi.org/10.1007/s12012-024-09956-0","url":null,"abstract":"Atherosclerosis risk is elevated in diabetic patients, but the underlying mechanism such as the involvement of macrophages remains unclear. Here, we investigated the underlying mechanism related to the pro-inflammatory activation of macrophages in the development of diabetic atherosclerosis. Bioinformatics tools were used to analyze the macrophage-related transcriptome differences in patients with atherosclerosis and diabetic mice. LDLR-/- mice with DDIT4 depletion were generated and fed a Western diet to induce atherosclerosis. DDIT4 expression was elevated in diabetic mice and patients with atherosclerosis. Macrophage proinflammatory factors F4/80, Il-6, and TNFα were reduced in DDIT4-/-LDLR-/- mice and necrotic areas were decreased in the aortic root. Atherosclerotic plaque stability was increased in DDIT4-/-LDLR-/- mice, as evidenced by increased collagen and smooth muscle cell content. DDIT4, regulated by ETV5, acted on macrophages, affecting lipid accumulation, migration capacity, and pro-inflammatory responses. Knockdown of ETV5 increased expression of DDIT4 and pro-inflammatory factors in macrophages, increased necrotic core area in the aortic root, and decreased stability of atherosclerotic plaques in mice, which was abated by DDIT4 knockdown. The findings provide new insight into how diabetes promotes atherosclerosis and support a model wherein loss of ETV5 sustains transcription of DDIT4 and the pro-inflammatory activation of macrophages.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037239","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}

引用次数: 0

Pregnancy and Postpartum Effects of Electronic Cigarettes on Maternal Health and Vascular Function in the Fourth Trimester. 孕期和产后电子烟对妊娠晚期产妇健康和血管功能的影响。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-22 DOI: 10.1007/s12012-025-09961-x

Amber Mills, Duaa Dakhlallah, Anand Ranpara, W Travis Goldsmith, Paul D Chantler, Yue-Wern Huang, Jonathan Boyd, I Mark Olfert

{"title":"Pregnancy and Postpartum Effects of Electronic Cigarettes on Maternal Health and Vascular Function in the Fourth Trimester.","authors":"Amber Mills, Duaa Dakhlallah, Anand Ranpara, W Travis Goldsmith, Paul D Chantler, Yue-Wern Huang, Jonathan Boyd, I Mark Olfert","doi":"10.1007/s12012-025-09961-x","DOIUrl":"https://doi.org/10.1007/s12012-025-09961-x","url":null,"abstract":"Pregnancy is a vulnerable time with significant cardiovascular changes that can lead to adverse outcomes, which can extend into the postpartum window. Exposure to emissions from electronic cigarettes (Ecig), commonly known as \"vaping,\" has an adverse impact on cardiovascular function during pregnancy and post-natal life of offspring, but the postpartum effects on maternal health are poorly understood. We used a Sprague Dawley rat model, where pregnant dams are exposed to Ecigs between gestational day (GD)2-GD21 to examine postpartum consequences. Litter and dam health were monitored during the weaning period, and maternal vascular and endocrine function were assessed after weaning. Exposure to Ecig emissions during pregnancy led to fetal losses (i.e., reabsorption in utero) and reduced survival of pups during weaning compared to controls (air-exposed dams). We find that maternal vaping during pregnancy, with or without nicotine (or flavoring) results in maternal vascular and hormonal dysfunction (i.e., reduced prolactin, increased expression of sirtuin 1 deacetylase in the brain). Both 5 and 30W Ecig aerosol exposures resulted in significant impairment of middle cerebral artery reactivity to acetylcholine-mediated dilation (decreasing ~ 22 and ~ 50%, respectively). We also observed an increase in the number of extracellular vesicles (EVs) in plasma from 30-W group that persists up to 3-week postpartum and that these EVs impaired endothelial cell function when applied to in vitro and ex vivo assays. Our data suggest (1) Ecig vaping, even without nicotine or flavorings, during pregnancy alters maternal circulating factors that influence maternal and fetal health, (2) circulating EVs may contribute to the etiology of vascular dysfunction, and (3) that the window for recovery from vascular dysfunction in the dam is likely to be longer than the exposure window.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000497","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}

引用次数: 0

In Utero Nano-Titanium Dioxide Exposure Results in Sexually Dimorphic Weight Gain and Cardiovascular Function in Offspring. 子宫内纳米二氧化钛暴露导致后代性别二态性体重增加和心血管功能。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-21 DOI: 10.1007/s12012-025-09960-y

Russell Hunter, Teresa Gluth, Ethan Meadows, Riley Nett, Victoria Nist, Elizabeth Bowdridge

{"title":"In Utero Nano-Titanium Dioxide Exposure Results in Sexually Dimorphic Weight Gain and Cardiovascular Function in Offspring.","authors":"Russell Hunter, Teresa Gluth, Ethan Meadows, Riley Nett, Victoria Nist, Elizabeth Bowdridge","doi":"10.1007/s12012-025-09960-y","DOIUrl":"https://doi.org/10.1007/s12012-025-09960-y","url":null,"abstract":"Engineered nanomaterials (ENM) are capable of crossing the placental barrier and accumulating in fetal tissue. Specifically, the ENM nano-titanium dioxide (nano-TiO2), has been shown to accumulate in placental and fetal tissue, resulting in decreased birthweight in pups. Additionally, nano-TiO2 is an established cardiac toxicant and regulator of glucose homeostasis, and exposure in utero may lead to serious maladaptive responses in cardiac development and overall metabolism. The current study examines weight gain and cardiac function in male and female Sprague-Dawley rats exposed to 12 mg/m3 nano-TiO2 or filtered air for 6 non-consecutive days in utero between gestational days 12-19. These animals were randomly assigned to receive a grain-based or high-fat diet (60%) between postnatal weeks 12-24 to examine the propensity for weight gain and cardiac response as adults. Our results show a sexually dimorphic response to weight gain with male rats gaining more weight after high-fat diet following in utero nano-TiO2 exposure, and female rats gaining less weight on the high-fat diet respective of exposure. Male rats exposed to nano-TiO2 in utero had reduced ejection fraction prior to diet when compared to air controls. Female rats subjected to in utero nano-TiO2 exposure showed a significant decrease in cardiac output following 12 weeks of high-fat diet. Development of cardiovascular impairments and ultimately cardiac dysfunction and disease following in utero exposures highlights the need for occupational and environmental monitoring of nanoparticulate exposure.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000477","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}

引用次数: 0

Indoxyl Sulfate Induces Ventricular Arrhythmias Attenuated by Secretoneurin in Right Ventricular Outflow Tract Cardiomyocytes. 硫酸吲哚酚诱导右心室流出道心肌细胞分泌神经蛋白减弱室性心律失常。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-21 DOI: 10.1007/s12012-025-09963-9

Yuan Hung, Chen-Chuan Cheng, Yen-Yu Lu, Shih-Yu Huang, Yao-Chang Chen, Fong-Jhih Lin, Wei-Shiang Lin, Yu-Hsun Kao, Yung-Kuo Lin, Shih-Ann Chen, Yi-Jen Chen

{"title":"Indoxyl Sulfate Induces Ventricular Arrhythmias Attenuated by Secretoneurin in Right Ventricular Outflow Tract Cardiomyocytes.","authors":"Yuan Hung, Chen-Chuan Cheng, Yen-Yu Lu, Shih-Yu Huang, Yao-Chang Chen, Fong-Jhih Lin, Wei-Shiang Lin, Yu-Hsun Kao, Yung-Kuo Lin, Shih-Ann Chen, Yi-Jen Chen","doi":"10.1007/s12012-025-09963-9","DOIUrl":"https://doi.org/10.1007/s12012-025-09963-9","url":null,"abstract":"Ventricular arrhythmias (VAs) are major causes of sudden cardiac death in chronic kidney disease (CKD) patients. Indoxyl sulfate (IS) is one common uremic toxin found in CKD patients. This study investigated whether IS could induce VAs via increasing right ventricular outflow tract (RVOT) arrhythmogenesis. Using conventional microelectrodes and whole-cell patch clamps, we studied the action potentials (APs) and ionic currents of isolated rabbit RVOT tissue preparations and single cardiomyocytes before and after IS (0.1 and 1.0 μM). Calcium fluorescence imaging was performed in RVOT cardiomyocytes treated with and without IS (1.0 μM) to evaluate the calcium transient and the calcium leak. In rabbit RVOT tissues, IS (0.1 and 1.0 μM) attenuated the contractility and shortened the AP durations in a dose-dependent manner. In addition, IS (0.1 and 1.0 μM) enhanced the pro-arrhythmia effects of isoproterenol (ISO, 1.0 μM) and rapid ventricular pacing in RVOT (before versus after ISO, 25% versus 83%, N = 12). In RVOT cardiomyocytes, IS (1.0 μM) significantly decreased the L-type calcium currents but increased the sodium-calcium exchanger and sodium window currents. Cardiomyocytes treated with IS (1.0 μM) had lower calcium transients but higher diastolic calcium and calcium leak than those without IS treatment. Pretreatment with secretoneurin (SN, 30 nM, a potent neuropeptide, suppressing CaMKII) or KN-93 (0.1 μM, a CaMKII inhibitor) prevented IS-induced ionic current changes and arrhythmogenesis. In conclusion, IS modulates RVOT electrophysiology and arrhythmogenesis via enhanced CaMKII activity, which is attenuated by SN, leading to a novel therapeutic target for CKD arrhythmias.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000479","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}

引用次数: 0

NLRC5 in Macrophages Promotes Atherosclerosis in Acute Coronary Syndrome by Regulating STAT3 Expression. 巨噬细胞NLRC5通过调节STAT3表达促进急性冠脉综合征动脉粥样硬化。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-20 DOI: 10.1007/s12012-024-09957-z

Jun Chen, Guoqin Chen, Jianhao Li, Dayu Wang, Weijie Liang, Shanjun Zhao

{"title":"NLRC5 in Macrophages Promotes Atherosclerosis in Acute Coronary Syndrome by Regulating STAT3 Expression.","authors":"Jun Chen, Guoqin Chen, Jianhao Li, Dayu Wang, Weijie Liang, Shanjun Zhao","doi":"10.1007/s12012-024-09957-z","DOIUrl":"https://doi.org/10.1007/s12012-024-09957-z","url":null,"abstract":"The mortality rate of cardiovascular and cerebrovascular diseases ranks first among all causes. This study elucidated the role and potential mechanism of the NLRC5 gene in atherosclerosis (AS). We enrolled patients (number = 30) diagnosed with AS and healthy volunteers (number = 30) as controls from our hospital. In patients with AS, the levels of serum NLRC5 were up-regulated (Fig. 1A) and positively correlated with CIMT/CRP. In a mouse model of AS, the expression of serum NLRC5 mRNA was increased at 6 or 12 weeks after inducing AS. The expression of NLRC5 protein was found to be elevated in a mouse model of AS. The inhibition of NLRC5 reduced development of AS in ApoE-/- Mice. Reducing NLRC5 inhibited the polarization of M2 macrophages and shifted macrophages towards proinflammatory M1 phenotype. STAT3 was identified as a target of NLRC5, with NLRC5 protein expression shown to reduce STAT3 ubiquitination. Methylation promoted NLRC5 DNA stability in vitro model of AS. Sh-NLRC5 increased M1/M2 macrophage ratio, foam cell formation and ox-LDL uptake. STAT3 reduced the effects of sh-NLRC5-mediated M1/M2 macrophage ratio in model of AS. These data confirmed that NLRC5 in macrophages promotes atherosclerosis in acute coronary syndrome by regulating STAT3 expression. This suggests that NLRC5 could be a potential target for the treatment of premature AS.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000493","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}

引用次数: 0

Taxifolin Protects Against 5-Fluorouracil-Induced Cardiotoxicity in Mice Through Mitigating Oxidative Stress, Inflammation, and Apoptosis: Possible Involvement of Sirt1/Nrf2/HO-1 Signaling. Taxifolin通过减轻氧化应激、炎症和细胞凋亡，保护小鼠免受5-氟尿嘧啶诱导的心脏毒性：可能参与Sirt1/Nrf2/HO-1信号传导

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-19 DOI: 10.1007/s12012-025-09962-w

Mohammad H Abukhalil, Zina Al-Alami, Manal A Alfwuaires, Mohd Rasheeduddin Imran, Saleem H Aladaileh, Osama Y Althunibat

{"title":"Taxifolin Protects Against 5-Fluorouracil-Induced Cardiotoxicity in Mice Through Mitigating Oxidative Stress, Inflammation, and Apoptosis: Possible Involvement of Sirt1/Nrf2/HO-1 Signaling.","authors":"Mohammad H Abukhalil, Zina Al-Alami, Manal A Alfwuaires, Mohd Rasheeduddin Imran, Saleem H Aladaileh, Osama Y Althunibat","doi":"10.1007/s12012-025-09962-w","DOIUrl":"https://doi.org/10.1007/s12012-025-09962-w","url":null,"abstract":"Although 5-fluorouracil (5-FU) is widely utilized in cancer treatment, its side effects, including cardiotoxicity, limit its use. Taxifolin (TAX) is a bioactive anti-inflammatory and antioxidant flavonoid. This study aimed to elucidate the protective effect of TAX against 5-FU-induced cardiac injury in male mice. Mice were treated with TAX (25 and 50 mg/kg, orally) for 10 days and a single dose of 150 mg/kg 5-FU at day 8. Mice intoxicated with 5-FU showed increased creatine kinase-MB and lactate dehydrogenase activities and troponin I levels, with multiple cardiac histopathological changes. They also showed a significant increase in cardiac malondialdehyde (MDA) and nitric oxide (NO) and decreases in myocardial reduced glutathione (GSH) content and superoxide dismutase (SOD) and catalase (CAT) activities (P < 0.001). Pretreatment of 5-FU-injected mice with TAX suppressed cardiac injury, decreased MDA and NO contents (P < 0.001), and boosted antioxidant defenses in the myocardium. Moreover, TAX attenuated cardiac inflammatory response, as evidenced by the decreased expression levels of cardiac NF-κB p65, inducible nitric oxide synthase (iNOS), and pro-inflammatory cytokines (P < 0.001). Largely, TAX ameliorated the decrease in Bcl-2 expression and the increase in BAX and caspase-3 in the heart. It also restored the cardiac Sirt1/Nrf2/HO-1 signaling pathway. In conclusion, TAX showed significant cardioprotective effects on 5-FU-induced cardiac injury and might represent a promising adjuvant in preventing cardiac injury associated with oxidative stress and inflammation.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000623","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}

引用次数: 0

Cohort Studies and Multi-omics Approaches to Low-Dose Ionizing Radiation-Induced Cardiovascular Disease: A Comprehensive Review. 针对低剂量电离辐射诱发心血管疾病的队列研究和多组学方法：全面回顾。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-01 Epub Date: 2024-11-13 DOI: 10.1007/s12012-024-09943-5

Xumin Zong, Lin Zhu, Yan Wang, Jinhan Wang, Yeqing Gu, Qiang Liu

{"title":"Cohort Studies and Multi-omics Approaches to Low-Dose Ionizing Radiation-Induced Cardiovascular Disease: A Comprehensive Review.","authors":"Xumin Zong, Lin Zhu, Yan Wang, Jinhan Wang, Yeqing Gu, Qiang Liu","doi":"10.1007/s12012-024-09943-5","DOIUrl":"10.1007/s12012-024-09943-5","url":null,"abstract":"The effect of low-dose ionizing radiation exposure on the risk of cardiovascular disease (CVD) represents a significant concern in the field of radiation protection. The prevailing approach to mitigating the adverse effects of low-dose or low-dose-rate radiation does not currently incorporate the potential risk of CVD, despite the possibility that such risk may be a substantial contributor to overall health hazards. Current evidence suggests a potential association between radiation exposure and CVD; however, the overall findings remain inconclusive. This is particularly due to the uncertainty surrounding the influence of significant non-radiation risk factors on the associations reported in epidemiological studies. It is difficult to discern the underlying connection in observational epidemiology when there is substantial variation in baseline risk factors. The paucity of epidemiological research in this domain is being partially offset by the advancement of multi-omics approaches. These methods assist in identifying radiosensitive targets, comprehending underlying biological processes, and pinpointing biomarkers. This, in turn, fortifies the evidence gleaned from epidemiological studies. In this review, we delve into the body of epidemiological research pertaining to CVD induced by low-dose ionizing radiation and the application of multi-omics techniques. The integration of these two methodologies holds the promise of identifying specific molecules or biological pathways that can be employed to validate endpoints related to radiation risk assessment.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"148-165"},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615308","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}

引用次数: 0

Metagenomic Analysis of Gut Microbiome of Persistent Pulmonary Hypertension of the Newborn. 新生儿顽固性肺动脉高压肠道微生物组的元基因组分析

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-01 Epub Date: 2024-12-16 DOI: 10.1007/s12012-024-09949-z

Linli Han, Chuyang Lin, Yue Lan, Yimin Hua, Jinlin Wu, Zhenxin Fan, Yifei Li

{"title":"Metagenomic Analysis of Gut Microbiome of Persistent Pulmonary Hypertension of the Newborn.","authors":"Linli Han, Chuyang Lin, Yue Lan, Yimin Hua, Jinlin Wu, Zhenxin Fan, Yifei Li","doi":"10.1007/s12012-024-09949-z","DOIUrl":"10.1007/s12012-024-09949-z","url":null,"abstract":"Persistent pulmonary hypertension of the newborn (PPHN) is one of the most common diseases in the neonatal intensive care unit which severely affects neonatal survival. Gut microbes play an increasingly important role in human health, but there are rarely reported how gut microbiota contribute to PPHN. In our study, the metagenomic sequencing of feces from 12 PPHN's neonates and 8 controls were performed to expose the relation between neonatal gut microbes and PPHN disease. Firstly, we found that the abundance of Actinobacteria, Proteobacteria, Bacteroidetes were significantly increased in PPHN compared with controls, but the Firmicutes components was reduced. And some pathogenic strains (like Vibrio metschnikovii) were significantly enriched in the PPHN compared with controls. Secondly, functional annotation of genes found that PPHN up-regulated transmembrane transport, but down-regulated ribosome and ATP binding. Lastly, microbial metabolic pathway enrichment analysis indicated that some metabolic pathway in PPHN were conflicting and contradictory, showed that an abnormally increased metabolism, disturbed protein synthesis and genomic instability in the PPHN neonate. Our results contribute to understanding the changes in the species and function of gut microbiota in PPHN, thus providing a theoretical basis for the explanation and treatment of PPHN.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"135-147"},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827535","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}

引用次数: 0

Vascular Stress Markers Following Inhalation of Heated Tobacco Products: A Study on Extracellular Vesicles. 吸入加热烟草制品后的血管应激标志物：细胞外囊泡研究。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-01 Epub Date: 2024-10-29 DOI: 10.1007/s12012-024-09934-6

Lukasz Antoniewicz, Georgy Melnikov, Gustaf Lyytinen, Anders Blomberg, Jenny A Bosson, Linnea Hedman, Fariborz Mobarrez, Magnus Lundbäck

{"title":"Vascular Stress Markers Following Inhalation of Heated Tobacco Products: A Study on Extracellular Vesicles.","authors":"Lukasz Antoniewicz, Georgy Melnikov, Gustaf Lyytinen, Anders Blomberg, Jenny A Bosson, Linnea Hedman, Fariborz Mobarrez, Magnus Lundbäck","doi":"10.1007/s12012-024-09934-6","DOIUrl":"10.1007/s12012-024-09934-6","url":null,"abstract":"The advent of heated tobacco products (HTPs) has introduced new variables in the study of nicotine delivery systems and their health implications. Amidst concerns over cardiovascular effects, this study aims to elucidate the acute impact of HTP inhalation on extracellular vesicles (EV) levels in young, healthy individuals. In this controlled, acute exposure study, 23 young, healthy volunteers were subjected to HTP inhalation. EV levels of endothelial and platelet origin were quantified through flow cytometry before and after exposure. Data analysis was performed using multiple measures ANOVA to assess changes in EV concentrations. Our findings reveal a significant increase in EVs of endothelial and platelet origin following short-term HTP inhalation with nicotine. Notably, no significant change was observed in leukocyte- and neutrophil-derived EVs. This increase in EVs suggests acute vascular stress, with peak levels observed 4 h post-exposure. The rise in endothelial and platelet-derived EVs aligns with documented responses to acute vascular injury, paralleling the effects seen with traditional cigarette and e-cigarette use. Despite HTPs being marketed as safer alternatives, our results indicate that nicotine-containing HTPs may still pose significant vascular risks. These findings contribute to the growing body of evidence cautioning against the perceived safety of HTPs and reinforce the importance of regulatory oversight and public health initiatives targeting nicotine delivery technologies. Trial Registrations: ClinicalTrials.gov ID: NCT04824495, registered 2021-01-07.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"1-8"},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11739193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543915","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}

引用次数: 0

Persistent Ferroptosis Modulates Cardiac Remodeling and M2 Macrophage Polarization, Which Can be Mitigated by Astaxanthin During Myocardial Infarction Recovery. 在心肌梗死恢复过程中，虾青素可缓解持续性铁中毒对心脏重塑和 M2 巨噬细胞极化的调节作用。

IF 3.4 3区医学

Cardiovascular Toxicology Pub Date : 2025-01-01 Epub Date: 2024-11-04 DOI: 10.1007/s12012-024-09942-6

Cheng Shen, Yanian Wei, Wen Kang, Qianwen Wang, Guoqiang Li, Xin Chen, Long Wang

{"title":"Persistent Ferroptosis Modulates Cardiac Remodeling and M2 Macrophage Polarization, Which Can be Mitigated by Astaxanthin During Myocardial Infarction Recovery.","authors":"Cheng Shen, Yanian Wei, Wen Kang, Qianwen Wang, Guoqiang Li, Xin Chen, Long Wang","doi":"10.1007/s12012-024-09942-6","DOIUrl":"10.1007/s12012-024-09942-6","url":null,"abstract":"The role of ferroptosis, an iron-dependent lipid peroxidation regulated cell death pathway, remains obscure during myocardial infarction (MI) recovery. Our study aims to clarify ferroptosis' function in post-MI cardiac recovery, explore the consequences of iron overload and ferroptosis for myocardial remodeling, and assess the effects of Liproxstatin-1 (Lipro-1) treatment on macrophage functionality. Moreover, we examine the potential of Astaxanthin (ASTX), recognized for its antioxidative properties, to mitigate ferroptosis during MI recovery and its subsequent ramifications for myocardial remodeling. Our results demonstrate persistent ferroptosis during MI recovery, marked by decreased Glutathione Peroxidase 4 and increased Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4) and Ferroportin 1 alongside elevated lipid peroxidation and iron levels up to D21. We identified a significant correlation between ferroptosis and macrophage activity, noted by the increase in macrophage populations co-expressing GPX4 and ACSL4 markers in the peri-infarct area by D21. Liproxstatin-1 treatment reduced macrophage (CD68 +) counts, promoted M2 polarization decreased inflammation, and improved cardiac function. Myocardial remodeling was improved in Lipro-1-treated rats, as shown by decreased fibrosis and reduced levels of α-SMA, Collagen I, and Collagen III proteins. ASTX treatment also exhibited an inhibiting effect on ferroptosis indicators, and encouraged M2 macrophage polarization, reduced inflammation, and enhanced both cardiac function and myocardial remodeling, mirroring the beneficial effects observed with Lipro-1. In summary, the interactions between ferroptosis, macrophage polarization, and myocardial remodeling are crucial for cardiac function improvement post-MI. Lipro-1 and ASTX emerge as promising therapeutic agents by modulating post-MI ferroptosis and related immune responses.","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"58-73"},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567352","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}

引用次数: 0