Cardiovascular Toxicology最新文献

{"title":"Shen-fu Injection Modulates HIF- 1α/BNIP3-Mediated Mitophagy to Alleviate Myocardial Ischemia-Reperfusion Injury.","authors":"Zhian Chen, Tianying Liu, Lihui Xiong, Zhi Liu","doi":"10.1007/s12012-025-09993-3","DOIUrl":"10.1007/s12012-025-09993-3","url":null,"abstract":"<p><p>Coronary reperfusion therapy is the most common surgical treatment for myocardial infarction, but it can further induce myocardial ischemia-reperfusion injury (MIRI). Therefore, MIRI following coronary intervention is a challenging clinical issue. This study aims to investigate the involvement of HIF- 1α/BNIP3-mediated mitophagy in the protective effects of Shen-fu Injection (SFI) on MIRI in rats. Key targets and signaling pathways of myocardial MIRI were analyzed using high-throughput transcriptome data from the GSE240842 dataset in the GEO database.To establish the MIRI rat model, the left anterior descending coronary artery was ligated for 30 min, followed by reperfusion for 120 min. Hypoxia/reoxygenation (H/R) in neonatal rat primary cardiomyocytes was induced by oxygen-glucose deprivation for 4 h, followed by reoxygenation for 2 h. Two hours after reperfusion, assessments included myocardial infarction area, CK-MB, CTnI, HE staining, TUNEL, mitochondrial ultrastructure and autophagosomes, HIF- 1α, BNIP3, LC3B-II, LC3B-I protein expression, immunofluorescence, and qRT-PCR. Cardiac function was also evaluated using M-mode ultrasound 2 h after reperfusion. In cardiomyocytes, CCK- 8, EdU cell proliferation levels, scratch assay, mitochondrial membrane potential, ROS levels, cardiomyocyte apoptosis, protein expression levels, and immunofluorescence were assessed 2 h after reoxygenation. Our results indicate that HIF- 1α and BNIP3 are key targets in MIRI. SFI upregulates HIF- 1α expression, promoting moderate mitophagy. This process clears excessively damaged mitochondria, reduces cardiomyocyte apoptosis, and decreases myocardial injury. Additionally, SFI reduces autophagosome accumulation, lowers ROS production, and stabilizes membrane potential. Consequently, the area of myocardial infarction is reduced, and cardiac function is improved. SFI activates the HIF- 1α/BNIP3 pathway to mediate moderate mitophagy, effectively reducing cardiomyocyte apoptosis and alleviating myocardial ischemia-reperfusion injury, thereby protecting cardiomyocytes.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"898-914"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981158","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":"Membrane Protein of SARS-CoV-2 Promotes the Production of CXCL10 and Apoptosis of Myocardial Cells.","authors":"Xiaoguang Wu, Lu Tang, Wen Huang, Min Gao, Changhao Xu, Peng Li, Xiangqing Kong","doi":"10.1007/s12012-025-10001-x","DOIUrl":"10.1007/s12012-025-10001-x","url":null,"abstract":"<p><p>SARS-CoV-2 infections directly or indirectly cause unconscionable vascular events, significantly increasing the morbidity and mortality of COVID-19. Biomarkers associated with cardiac injury often elevate in individuals with COVID-19. Cytokine storm is a mechanism underlying myocardial cell injury caused by SARS-CoV-2 infections. Cell apoptosis in AC16 cells overexpressing structural and helper proteins of SARS-CoV-2 was detected by Western blot, MTT and TUNEL assay. The M protein was determined to play the most pronounced role in inducing apoptosis. Transcriptome sequencing on AC16 cells overexpressing the M protein was performed to screen differentially expressed genes (DEGs), which were further subjected to the gene set enrichment analysis. The regulatory effect of CXCL10 on cell apoptosis of AC16 cells overexpressing M protein was finally explored. Overexpression of M protein significantly increased the Bax/Bcl-2 and cleaved caspase-3/caspase-3(CC3/C3) ratios and the percentage of TUNEL-positive cells in AC16 cells, while markedly reducing cell viability. CXCL10 was the most prominent DEG in AC16 cells overexpressing M protein. Knockdown of CXCL10 partially reversed the increases in the Bax/Bcl-2 and cleaved caspase-3/caspase-3 ratios, the percentage of TUNEL-positive cells, as well as the release of pro-inflammatory cytokines in AC16 cells overexpressing M protein. The M protein of SARS-CoV-2 triggers the production of CXCL10 and apoptosis of myocardial cells.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"830-840"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981647","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":"Essential and Non-Essential Metals and Metalloids and Their Role in Atherosclerosis.","authors":"Pierce L Massie, Marcus Garcia, Aerlin Decker, Rui Liu, Milad MazloumiBakhshayesh, Deepali Kulkarni, Matthew P Justus, Jorge Gallardo, Avalon Abrums, Kristin Markle, Carolyn Pace, Matthew Campen, Ross M Clark","doi":"10.1007/s12012-025-09998-y","DOIUrl":"10.1007/s12012-025-09998-y","url":null,"abstract":"<p><p>Peripheral arterial disease (PAD) is becoming more prevalent in the aging developed world and can have significant functional impacts on patients. There is a recent recognition that environmental toxicants such as circulating metals and metalloids may contribute to the pathogenesis of atherosclerotic disease, but the mechanisms are complex. While the broad toxic biologic effects of metals in human systems have been extensively reviewed, the role of non-essential exposure and essential metal aberrancy in PAD specifically is less frequently discussed. This review of the literature describes current scientific knowledge regarding the individual roles several major metals and metalloids play in atherogenesis and highlights areas where a dearth of data exist. The roles of lead (Pb), arsenic (As), cadmium (Cd), iron (Fe), copper (Cu), selenium (Se) are included. Contemporary outcomes of therapeutic trials aimed at chelation therapy of circulating metals to impact cardiovascular outcomes are also discussed. This review highlights the supported notion of differential metal presence within peripheral plaques themselves, although distinguishing their roles within these plaques requires further illumination.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"841-866"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978792","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":"Protein Kinase C Epsilon Overexpression Protects the Heart Against Doxorubicin-Induced Cardiotoxicity Via Activating SIRT1.","authors":"Danyong Liu, Chunyan Wang, Yao Chen, Xiaolei Huang, Yajie Wen, Shan Duan, Yin Cai, Xia Li, Jianfeng He, Kaijia Han, Ting Li, Yuantao Li, Zhengyuan Xia","doi":"10.1007/s12012-025-09995-1","DOIUrl":"10.1007/s12012-025-09995-1","url":null,"abstract":"<p><p>Doxorubicin (DOX)-induced cardiotoxicity (DIC) is known to be associated with reduction of cardiac protein kinase C epsilon (PKC-ε). PKC-ε promotes cell survival and protects hearts against various stresses. However, it is unclear whether or not the reduction in cardiac PKC-ε expression plays a causal role in DIC and in particular the potential underlying mechanism whereby PKC-ε may protect against DIC. C57BL/6 mice (8-10-week-old) were either treated with DOX administered intraperitoneally for a duration of 4 weeks to produce cardiotoxicity, or untreated in which mice received the same volume of saline. In vitro, neonatal rat ventricle cardiomyocytes were exposed to DOX for 24 h in the absence or presence of adenovirus overexpressing PKC-ε. Cardiomyocytes in a subgroup were treated with sirtuin-1 (SIRT1) selective inhibitor Ex527. Four weeks after DOX, cardiac contractile function was decreased concomitant with increased serum CK-MB and LDH levels as well as increases in Bax-to-Bcl-2 ratio and Cleaved Caspase 3 proteins expression, while PKC-ε and Sirt1 protein expressions were significantly decreased. In vitro, DOX reduced cardiomyocyte PKC-ε and SIRT1 protein expression, decreased cardiomyocyte viability, and increased LDH release with concomitant increases in oxidative stress and apoptosis. These changes were attenuated by overexpression of PKC-ε. IP study showed that PKC-ε could directly or indirectly bind SIRT1 in cardiomyocytes, and the protect effects of PKC-ε were further canceled by SIRT1 inhibition. In conclusion, activating SIRT1 may represent a major mechanism whereby PKC-ε protects the heart against DOX-induced cell apoptosis and oxidative stress.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"915-928"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12116906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981155","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":"Association Between the Uric Acid to High-Density Lipoprotein Cholesterol Ratio and Residual Risk for Coronary Artery Disease.","authors":"Shan Zhong, Siqi Wang, Peng Zhao, Minghui Piao, Cheng Jin, Jinwei Tian","doi":"10.1007/s12012-025-10000-y","DOIUrl":"10.1007/s12012-025-10000-y","url":null,"abstract":"<p><p>Despite advances in anti-atherosclerotic therapies, residual risk persists in coronary artery disease (CAD). The uric acid to high-density lipoprotein cholesterol ratio (UHR), a metabolic-inflammatory marker, may predict residual risk, but its association with plaque progression remains unexplored. This study investigates the impact of UHR on atherosclerotic plaque burden in CAD patients after treatment. In this prospective cohort study, 118 patients with newly diagnosed CAD undergoing percutaneous coronary intervention were stratified into quartiles by baseline UHR. Intravascular ultrasound assessed plaque burden and characteristics at baseline and 12-month follow-up. Logistic regression and restricted cubic spline models evaluated associations between UHR and plaque progression, adjusting for cardiovascular risk factors. At baseline, the highest UHR quartile (UHR-4) exhibited higher rates of plaque rupture (19.6% vs. 0-8.7%, P = 0.002) and microchannels (56.5% vs. 33.3-55.3%, P = 0.031) compared to lower quartiles. Baseline percent atheroma volume (PAV) was greater in UHR-4 (52.73% vs. 51.04-52.09%, P = 0.006). At follow-up, UHR-4 had a 3.2-fold increased risk of plaque burden > 70% (adjusted RR 3.237, 95% CI 1.156-9.063, P = 0.025), with a linear UHR-plaque burden relationship (P = 0.015). No associations were observed between UHR and minimal lumen area or positive remodeling. Elevated UHR is independently associated with high atherosclerotic plaque burden (> 70%) in CAD patients under guideline-directed therapy after adjusting for traditional risk factors. UHR may serve as a complementary biomarker to existing risk scores, guiding targeted therapies to mitigate plaque vulnerability.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"874-883"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970727","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":"Impact of Gene-Smoking Interaction on Risk of Atherosclerosis: Molecular Study of Prothrombin (F2) Gene rs1799963 G/A Polymorphism in Atherosclerotic Patients.","authors":"Farrakh Ali Abbas, Shazia Batool, Moazma Hina, Tayyba Khalid, Amna Aman, Fazli Rabbi Awan, Misbah Hussain","doi":"10.1007/s12012-025-09997-z","DOIUrl":"10.1007/s12012-025-09997-z","url":null,"abstract":"<p><p>Atherosclerosis is a multifactorial disease influenced by genetic and lifestyle factors (e.g., smoking). The rs1799963 G/A polymorphism in the prothrombin (F2) gene is associated with thrombosis and cardiovascular diseases. However, the interaction between this genetic variant and smoking on the risk of atherosclerosis has not been thoroughly investigated. This study aims to explore the impact of rs1799963 polymorphism-smoking interaction on the risk of atherosclerosis. For this, control (n = 40) and angiographically confirmed atherosclerotic patients (n = 82) were recruited from District Sargodha, Pakistan. All subjects were genotyped for rs1799963 G/A variants by in-house developed tri-ARMS-PCR assay. Statistical analysis was performed to evaluate the interaction between rs1799963 polymorphism and smoking in relation to atherosclerosis risk. Risk of atherosclerosis was increased by the individual effects of F2 rs1799963 G allele [OR 2.96 (95% CI:1.8-8.08) p = 0.034] and smoking [OR 3.9 (95% CI:1.4-10.8) p = 0.008]. Subjects harboring rs1799963 G allele and who were active smokers had ~ 20 times higher risk of atherosclerosis. Synergy index indicated that combined effect of smoking and rs1799963 G allele was higher than their individual effects, which had a positive interaction with atherosclerosis [synergy index = 2.125 (95% CI: 1.66-2.59)]. These findings suggest a strong interaction between F2 rs1799963 polymorphism and smoking for atherosclerosis. The presence of rs1799963 G allele in conjunction with active smoking status greatly increases the risk of atherosclerosis.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"867-873"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967037","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":"COVID-19 Predisposition Inherently Increases Cardiovascular Risk Before SARS-CoV-2 Infection.","authors":"Ming Zheng","doi":"10.1007/s12012-025-09996-0","DOIUrl":"10.1007/s12012-025-09996-0","url":null,"abstract":"<p><p>As COVID-19 transitions to an endemic stage, its long-term impacts on health, particularly cardiovascular disease (CVD), remain significant. While prior studies have focused on cardiovascular complications following SARS-CoV-2 infection, the question of inherent cardiovascular risk associated with genetic predisposition to COVID-19 has been less explored. This study investigates whether individuals genetically predisposed to COVID-19 may also be at higher risk for CVD, independent of actual infection. Using Mendelian randomization (MR) analysis with data from pre-pandemic, SARS-CoV-2-naive populations, this study assessed the impact of genetic susceptibility to COVID-19 on various CVD outcomes across 18 distinct cohorts. This approach allowed us to simulate COVID-19 predisposition without infection, providing insights into cardiovascular risks associated solely with genetic susceptibility. These findings reveal a significant association between genetic predisposition to COVID-19 and elevated risks for several CVD outcomes, particularly hypertensive heart disease. Notably, individuals with a genetic profile linked to severe COVID-19 (hospitalization-prone) showed a marked increase in risk for hypertensive heart disease. These findings suggest a shared genetic architecture that predisposes individuals to both COVID-19 and cardiovascular risks, irrespective of viral exposure. COVID-19 susceptibility, thus, may act as a \"natural stress test,\" revealing latent cardiovascular vulnerabilities. This connection implies that individuals predisposed to severe COVID-19 may have inherently higher cardiovascular risks, even without SARS-CoV-2 infection. This study highlights the value of COVID-19 susceptibility as a novel marker for assessing CVD risk, enabling timely preventive strategies and mitigating future CVD burden in the post-COVID-19 era. Moreover, this study highlights disease predisposition as a \"black box\" until clinical onset. While COVID-19 demands an external viral trigger for acute onset, cardiovascular disease unfolds much more slowly, requiring prolonged exposure to detrimental lifestyle and genetic factors. Together, their intersection illustrates how acute environmental triggers and chronic disease processes can converge to influence overall health outcomes.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"821-829"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978862","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":"MiR214-3p Ameliorates Diabetic Cardiomyopathy by Inhibiting Ferroptosis.","authors":"Peng Chen, Xiaohui Huang, Weixing Wen, Yue Cao, Weiwen Li, Guolin Huang, Yuli Huang, Yunzhao Hu, Tianyi Ma","doi":"10.1007/s12012-025-09992-4","DOIUrl":"10.1007/s12012-025-09992-4","url":null,"abstract":"<p><p>Ferroptosis is involved in the pathogenesis of diabetic cardiomyopathy (DCM). It has been shown that miR214-3p regulates ferroptosis, but no studies have shown a relationship between miR214-3p and DCM. This study induced glucolipotoxicity cardiomyocytes by treating HL-1 with high glucose and palmitic acid. Under these conditions, intracellular proteins TfR1 and FTH1, involved in Fe²⁺ transport and storage, were significantly elevated, and intracellular Fe²⁺ deposition was increased. The expression of GPX4, a key antioxidant molecule in ferroptosis, was reduced considerably, and the expression of lipid peroxidation-related proteins ACSL4 and COX2 was significantly elevated, with increased intracellular lipid peroxidation. Glucolipotoxicity cardiomyocytes overexpressing miR214-3p showed reduced expression levels of intracellular iron metabolism-related proteins, decreased Fe²⁺ deposition, elevated GPX4 expression, markedly down-regulated expression of ACSL4 and COX2, and reduced intracellular lipid peroxidation. In contrast, glucolipotoxicity cardiomyocytes with knockdown of miR214-3p showed more severe Fe²⁺ deposition and lipid peroxidation. In vivo, DCM mice showed significant cardiac function reduction and myocardial fibrosis. Consistent with the in vitro experiments, the expression level of GPX4 in myocardial tissues of DCM mice was reduced, and the expression of FTH1, ACSL4, and COX2 was significantly elevated. In contrast, DCM mice treated with miR214-3p showed improved cardiac function and alleviated myocardial fibrosis, with up-regulated GPX4 protein expression levels and significantly suppressed FTH1, ACSL4, and COX2 expression. These findings revealed that miR214-3p inhibits ferroptosis to improve DCM.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"884-897"},"PeriodicalIF":3.4,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794678","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":"Association of VEGFA Gene Polymorphisms with the Susceptibility of Coronary Heart Disease in the Chinese Han Population.","authors":"Kang Huang, Shijuan Lu, Yilei Zhou, Dehong Lin, Zibin Chen, Zanrui Zhong, Jianghua Zhong","doi":"10.1007/s12012-025-10003-9","DOIUrl":"https://doi.org/10.1007/s12012-025-10003-9","url":null,"abstract":"<p><p>Coronary heart disease (CHD) is a prevalent cardiovascular' condition characterized by high morbidity and mortality rates, with a significant genetic component. The VEGFA gene plays a crucial role in the development of CHD. This study aims to evaluate the influence of VEGFA gene polymorphisms on CHD susceptibility. Peripheral blood samples were collected from 479 CHD patients and 479 healthy controls. We genotyped four VEGFA single nucleotide polymorphisms (SNPs): rs833068, rs833070, rs3025021, and rs3025030, using the Agena MassARRAY platform. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate the association between these SNPs and CHD risk. Multifactor dimensionality reduction (MDR) was employed to analyze potential SNP-SNP interactions. The rs833068 SNP was found to be associated with a reduced risk of CHD (OR 0.46, p = 0.013), whereas the rs3025021 (OR 1.32, p = 0.031) and rs3025030 (OR 1.30, p = 0.032) SNPs were linked to an increased risk. The stratified analysis revealed that rs833068 decreased CHD risk in individuals aged < 61 years, those with a BMI ≥ 24, non-smokers, non-drinkers, and patients with diabetes, but increased the risk in hypertensive individuals. The rs833070 SNP significantly increased CHD risk in non-smokers and non-drinkers. Rs3025021 was associated with an increased CHD risk in subjects with a BMI < 24, smokers, drinkers, and diabetics. Rs3025030 was found to increase CHD susceptibility in aged > 61 years, males, those with a BMI ≥ 24, and drinkers. MDR analysis identified a combination of rs833068, rs3025021, and rs3025030 as the most predictive model for CHD. Polymorphisms in the VEGFA gene are associated with CHD risk in the Chinese Han population, offering a novel perspective for CHD diagnosis.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186646","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":"Radiation-Induced Cardiac Remodeling: Mechanisms and Therapeutic Approaches.","authors":"Zahraa Sabah Ghnim, Ayat Hussein Adhab, Morug Salih Mahdi, Ashishkumar Kyada, R Roopashree, Vishal Thakur, Manpreet Kaur, Anirudh Gupta, Aseel Salah Mansoor, Usama Kadem Radi, Nasr Saadoun Abd, Munther Kadhim","doi":"10.1007/s12012-025-10006-6","DOIUrl":"https://doi.org/10.1007/s12012-025-10006-6","url":null,"abstract":"<p><p>Radiation-induced cardiac remodeling (RICR) is one of the complications of exposure to radiotherapy. These disorders may occur for a subset of cancer patients, when the heart remains in part or in full in the radiation field. Despite advancements in radiotherapy techniques, cardiotoxicity has remained a concern after radiotherapy. RICR includes complex pathophysiological processes, which can be initiated by oxidative stress and cardiomyocyte cell death and continue with inflammation, arrhythmia, vascular and valvular abnormalities, and fibrosis, collectively contributing to structural and functional changes in the heart. Some studies have suggested strategies for RICR encompass pharmacological interventions, including angiotensin-converting enzyme (ACE) inhibitors, natural products, antioxidants, and others, which aim to mitigate cardiac damage and improve outcomes. Advanced therapies, including stem cell and gene therapy, as well as some adjuvants and novel drugs targeting specific molecular pathways, represent future directions for treatment. This review aims to elucidate the mechanisms underlying RICR, highlight early detection strategies, and discuss current and emerging therapeutic approaches.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172668","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}