Journal of Cardiovascular Translational Research最新文献

筛选
英文 中文
NAT10 Modulates Atherosclerosis Progression Mediated by Macrophage Polarization Through Regulating ac4C Modification of TLR9.
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-19 DOI: 10.1007/s12265-024-10579-7
Wei Yin, Jie Wang, Lingling Li, Hongyun Zheng, Shengkai Xu
{"title":"NAT10 Modulates Atherosclerosis Progression Mediated by Macrophage Polarization Through Regulating ac4C Modification of TLR9.","authors":"Wei Yin, Jie Wang, Lingling Li, Hongyun Zheng, Shengkai Xu","doi":"10.1007/s12265-024-10579-7","DOIUrl":"https://doi.org/10.1007/s12265-024-10579-7","url":null,"abstract":"<p><p>Atherosclerosis (AS) is an inflammatory disease affected by macrophage polarization. N<sup>4</sup>-acetylcytosine (ac4C) modification mediated by N-acetyltransferase 10 (NAT10). In this study, we aimed to elucidate the role of ac4C modification mediated macrophage polarization in AS through in vivo and in vitro experiments. The ac4C level was measured using dot blot. Macrophage polarization was assessed by quantitative real-time PCR and flow cytometry. Underlying mechanism was analyzed by methylated RNA Immunoprecipitation (MeRIP), RIP and dual luciferase report. Results showed that the NAT10 expression and ac4C level were increased in patients with AS. Additionally, NAT10 knockdown promoted M1 to M2 polarization and suppressed TLR9 ac4C level. TLR9 overexpression reversed macrophage polarization regulated by NAT10 knockdown. Furthermore, M1 polarization and atherosclerosis in vivo was inhibited by NAT10 knockdown. In conclusion, we demonstrated that NAT10 regualted AS progression mediated by macrophage polarization through regulating ac4C modification of TLR9 and provided a new theoretical basis.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854279","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
Associations of Blood Lipid-Related Polygenic Scores, Lifestyle Factors and Their Combined Effects with Risk of Coronary Artery Disease in the UK Biobank Cohort. 英国生物库队列中血脂相关多基因评分、生活方式因素及其综合效应与冠状动脉疾病风险的关系。
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-16 DOI: 10.1007/s12265-024-10578-8
Jungyoon Choi, Wanqing Wen, Guochong Jia, Ran Tao, Jirong Long, Xiao-Ou Shu, Wei Zheng
{"title":"Associations of Blood Lipid-Related Polygenic Scores, Lifestyle Factors and Their Combined Effects with Risk of Coronary Artery Disease in the UK Biobank Cohort.","authors":"Jungyoon Choi, Wanqing Wen, Guochong Jia, Ran Tao, Jirong Long, Xiao-Ou Shu, Wei Zheng","doi":"10.1007/s12265-024-10578-8","DOIUrl":"10.1007/s12265-024-10578-8","url":null,"abstract":"<p><p>Circulating lipids play a crucial role in the development of coronary artery disease (CAD). However, it is unclear whether the genetic susceptibility to hyperlipidemia may interact with lifestyle factors in CAD risk. Using UK Biobank data from 328,606 participants, we evaluated combined effects of genetic susceptibility to hyperlipidemia and lifestyle factors with risk of CAD. We found that both blood lipid-related polygenic score (PGS) and healthy lifestyle score (HLS) are independently associated with CAD risk, and individuals with the highest-risk lipid-related PGS and the least healthy HLS had the highest CAD risk. This association was stronger in younger (< 60 years, hazard ratio: 4.46, 95% confidence interval: 3.44-5.78) than older adults (2.54, 2.13-3.03). Our study suggests that individuals, particularly younger adults, with higher-risk PGSs of blood lipid traits would benefit more substantially by adherence to a healthy lifestyle than those with lower PGSs.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828606","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
Prediction of Major Adverse Limb Events in Females with Peripheral Artery Disease using Blood-Based Biomarkers and Clinical Features.
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-06 DOI: 10.1007/s12265-024-10574-y
Ben Li, Hamzah Khan, Farah Shaikh, Abdelrahman Zamzam, Rawand Abdin, Mohammad Qadura
{"title":"Prediction of Major Adverse Limb Events in Females with Peripheral Artery Disease using Blood-Based Biomarkers and Clinical Features.","authors":"Ben Li, Hamzah Khan, Farah Shaikh, Abdelrahman Zamzam, Rawand Abdin, Mohammad Qadura","doi":"10.1007/s12265-024-10574-y","DOIUrl":"https://doi.org/10.1007/s12265-024-10574-y","url":null,"abstract":"<p><p>The objective of this study was to identify a female-specific prognostic biomarker for peripheral artery disease (PAD) and develop a prediction model for 2-year major adverse limb events (MALE). Patients with/without PAD were recruited (n=461). Plasma concentrations of 68 circulating proteins were measured and patients were followed for 2 years. The primary outcome was MALE (composite of vascular intervention, major amputation, or acute/chronic limb threatening ischemia). We trained a random forest model using: 1) clinical characteristics, 2) female-specific PAD biomarker, and 3) clinical characteristics and female-specific PAD biomarker. Galectin-9 was the only protein to be significantly elevated in females compared to males in the discovery/validation analyses. The random forest model achieved the following AUROC's: 0.72 (clinical features), 0.83 (Galectin-9), and 0.86 (clinical features + Galectin-9). We identified Galectin-9 as a female-specific PAD biomarker and developed an accurate prognostic model for 2-year MALE using a combination of clinical features and plasma Galectin-9 levels.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791801","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
Endothelial Cell-Derived Extracellular Vesicles Allow to Differentiate Between Various Endotypes of INOCA: A Multicentre, Prospective, Cohort Study.
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-05 DOI: 10.1007/s12265-024-10575-x
Aleksandra Gąsecka, Piotr Szolc, Edwin van der Pol, Łukasz Niewiara, Bartłomiej Guzik, Paweł Kleczyński, Mariusz Tomaniak, Emilia Figura, Mateusz Zaremba, Marcin Grabowski, Janusz Kochman, Jacek Legutko, Łukasz Kołtowski
{"title":"Endothelial Cell-Derived Extracellular Vesicles Allow to Differentiate Between Various Endotypes of INOCA: A Multicentre, Prospective, Cohort Study.","authors":"Aleksandra Gąsecka, Piotr Szolc, Edwin van der Pol, Łukasz Niewiara, Bartłomiej Guzik, Paweł Kleczyński, Mariusz Tomaniak, Emilia Figura, Mateusz Zaremba, Marcin Grabowski, Janusz Kochman, Jacek Legutko, Łukasz Kołtowski","doi":"10.1007/s12265-024-10575-x","DOIUrl":"https://doi.org/10.1007/s12265-024-10575-x","url":null,"abstract":"<p><p>Ischemia and non-obstructive coronary artery disease (INOCA) might be due to coronary microvascular dysfunction (CMD), vasospastic angina (VSA) or both. We compared plasma concentration of various extracellular vesicles (EVs) in patients with different INOCA endotypes. Patients were divided into those with INOCA (CMD, VSA, mixed CMD + VSA) and non-anginal chest pain. Plasma concentrations of EVs were measured using flow cytometry. Out of 96 patients included, 34 had CMD (35%), 15 VSA (16%), 24 mixed endotype (25%) and 23 non-anginal chest pain (24%). Patients with INOCA had lower ratio of endothelial EVs (CD144 +) to total EVs, compared to patients with non-anginal pain (p = 0.027). Patients with mixed endotype had lower ratio of endothelial EVs (CD144 +) to total EVs, compared to CMD (p = 0.008), VSA (p = 0.014) and non-anginal pain (p < 0.001). Decreased ratio of endothelial EVs (CD144 +) to total EVs might serve as a \"circulating footprint\" of the mixed INOCA endotype.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785570","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
Gut Microbiota as Predictive Biomarker for Chronic Heart Failure in Patients with Different Nutritional Risk. 肠道微生物群作为不同营养风险患者慢性心力衰竭的预测性生物标志物
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-06-24 DOI: 10.1007/s12265-024-10529-3
Chen Yang, Xiaopeng Li, Miaomiao Hu, Ting Li, Li Jiang, Yong Zhang
{"title":"Gut Microbiota as Predictive Biomarker for Chronic Heart Failure in Patients with Different Nutritional Risk.","authors":"Chen Yang, Xiaopeng Li, Miaomiao Hu, Ting Li, Li Jiang, Yong Zhang","doi":"10.1007/s12265-024-10529-3","DOIUrl":"10.1007/s12265-024-10529-3","url":null,"abstract":"<p><p>To examine the relationship between gut microbiota and disease development in chronic heart failure patients with different nutritional risk. The study analyzed stool samples from 62 CHF patients and 21 healthy peoples using 16S rRNA gene sequencing. CHF patients were separated into risk (n = 30) and non-risk group (n = 32) based on NRS2002 scores. Analysis methods used were LEfSe, random forest regression model, ROC curves, BugBase, PICRUSt2, metagenomeSeq. Risk group includes 11 cases of HFrEF, 6 cases of HFpEF, and 13 cases of HFmrEF. LefSe analysis confirmed that the risk group had higher levels of Enterobacter and Escherichia-Shigella. Correlation analysis revealed a negative correlation between prealbumin and Escherichia-Shigella. The presence of Enterobacter and Escherichia-Shigella worsens intestinal inflammation in CHF patients, impacting lysine metabolism by influencing its degradation metabolic function. This interference further disrupts albumin and prealbumin synthesis, leading to malnutrition in CHF patients and ultimately worsening the disease.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1240-1257"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442761","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
Blood Pressure Variability After Non-invasive Low-level Tragus Stimulation in Acute Heart Failure. 急性心力衰竭患者接受非侵入性低水平外耳道刺激后的血压变化。
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-05 DOI: 10.1007/s12265-024-10544-4
Michiaki Nagai, Keigo Dote, Masaya Kato, Shota Sasaki, Noboru Oda, Sunny S Po, Tarun W Dasari
{"title":"Blood Pressure Variability After Non-invasive Low-level Tragus Stimulation in Acute Heart Failure.","authors":"Michiaki Nagai, Keigo Dote, Masaya Kato, Shota Sasaki, Noboru Oda, Sunny S Po, Tarun W Dasari","doi":"10.1007/s12265-024-10544-4","DOIUrl":"10.1007/s12265-024-10544-4","url":null,"abstract":"<p><p>Higher blood pressure (BP) variability (BPV) was shown to be strong predictors of poor cardiovascular outcomes in heart failure (HF). It is currently unknown if low-level tragus stimulation (LLTS) would lead to improvement in BPV in acute HF (AHF). The 22 patients with AHF (median 80 yrs, males 60%) were randomly assigned to active or sham group using an ear clip attached to the tragus (active group) or the earlobe (sham group) for 1 h daily over 5 days. In the active group, standard deviation (SD), coefficient of variation (CV) and δ in SBP were significantly decreased after LLTS (all p < 0.05). All the changes in SD, CV and δ in SBP before and after stimulation were also significantly different between active and sham groups (all p < 0.05). This proof-of-concept study demonstrates the beneficial effects of LLTS on BPV in AHF.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1347-1352"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141537953","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
HnRNPA1 Prevents Endothelial-to-mesenchymal Transition-induced VSMC Activation and Neointimal Hyperplasia in Vein Grafts. HnRNPA1 可防止内皮细胞向间质转化诱导的血管内皮细胞活化和静脉移植物的新内膜增生
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-24 DOI: 10.1007/s12265-024-10545-3
Haoliang Liu, Chaoqun Wang, Rui Wang, Yi Zhang, Bohao Jian, Zhuoming Zhou, Zhongkai Wu, Mengya Liang
{"title":"HnRNPA1 Prevents Endothelial-to-mesenchymal Transition-induced VSMC Activation and Neointimal Hyperplasia in Vein Grafts.","authors":"Haoliang Liu, Chaoqun Wang, Rui Wang, Yi Zhang, Bohao Jian, Zhuoming Zhou, Zhongkai Wu, Mengya Liang","doi":"10.1007/s12265-024-10545-3","DOIUrl":"10.1007/s12265-024-10545-3","url":null,"abstract":"<p><p>Endothelial-to-mesenchymal transition (EndoMT) is associated with neointimal hyperplasia and vein graft failure, and heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) has emerged as a major modulator of EMT. We aimed to investigate the functional consequence of EndoMT in neointimal hyperplasia and the precise role of hnRNPA1 in the regulation of EndoMT and neointimal hyperplasia. We investigated the spatial and temporal distribution characteristics of EndoMT cells in a mouse model of vein graft transplantation. In vitro, we studied the interaction between EndoMT cells and VSMCs, and the underlying mechanism was investigated by cytokine antibody assays. In cultured HUVECs, we studied the effect of hnRNPA1 on EndoMT and the cellular interactions by using siRNA-mediated knockdown and adenovirus-mediated overexpression. We further investigated the role of hnRNPA1 in EndoMT and neointimal hyperplasia in vivo with an AAV-mediated EC-specific hnRNPA1 overexpression murine model. We demonstrated the presence of EndoMT cells during the initial stage of neointimal formation, and that EndoMT cells promoted the proliferation and migration of VSMCs in vitro. Mechanistic studies revealed that EndoMT cells express and secrete a higher level of PDGF-B. Furthermore, we found a regulatory role for hnRNPA1 in EndoMT in vitro and in vivo. Similarly, we found that hnRNPA1 overexpression in ECs reduced the expression and secretion of PDGF-B during EndoMT, effectively inhibiting EndoMT cell-mediated activation of VSMCs in vitro and neointimal formation in vivo. Taken together, these findings indicate that EndoMT cells can activate VSMCs through a paracrine mechanism mediated by hnRNPA1 and lead to neointimal hyperplasia.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1400-1414"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751758","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
DDX17: A Potential Target for Heart Failure Therapies. DDX17:心力衰竭治疗的潜在靶点
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-29 DOI: 10.1007/s12265-024-10549-z
Wei Chen, Meiyu Hu, Juan Gao, Junjie Xiao
{"title":"DDX17: A Potential Target for Heart Failure Therapies.","authors":"Wei Chen, Meiyu Hu, Juan Gao, Junjie Xiao","doi":"10.1007/s12265-024-10549-z","DOIUrl":"10.1007/s12265-024-10549-z","url":null,"abstract":"","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1470-1472"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792529","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
Prediction of Left Ventricle Pressure Indices Via a Machine Learning Approach Combining ECG, Pulse Oximetry, and Cardiac Sounds: a Preclinical Feasibility Study. 通过结合心电图、脉搏氧饱和度和心音的机器学习方法预测左心室压力指数:临床前可行性研究。
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-17 DOI: 10.1007/s12265-024-10546-2
Lorenzo Fassina, Francesco Paolo Lo Muzio, Leonhard Berboth, Jens Ötvös, Alessandro Faragli, Alessio Alogna
{"title":"Prediction of Left Ventricle Pressure Indices Via a Machine Learning Approach Combining ECG, Pulse Oximetry, and Cardiac Sounds: a Preclinical Feasibility Study.","authors":"Lorenzo Fassina, Francesco Paolo Lo Muzio, Leonhard Berboth, Jens Ötvös, Alessandro Faragli, Alessio Alogna","doi":"10.1007/s12265-024-10546-2","DOIUrl":"10.1007/s12265-024-10546-2","url":null,"abstract":"<p><p>Heart failure (HF) is defined as the inability of the heart to meet body oxygen demand requiring an elevation in left ventricular filling pressures (LVP) to compensate. LVP increase can be assessed in the cardiac catheterization laboratory, but this procedure is invasive and time-consuming to the extent that physicians rather rely on non-invasive diagnostic tools. In this work, we assess the feasibility to develop a novel machine-learning (ML) approach to predict clinically relevant LVP indices. Synchronized invasive (pressure-volume tracings) and non-invasive signals (ECG, pulse oximetry, and cardiac sounds) were collected from anesthetized, closed-chest Göttingen minipigs. Animals were either healthy or had HF with reduced ejection fraction and circa 500 heartbeats were included in the analysis for each animal. The ML algorithm showed excellent prediction of LVP indices estimating, for instance, the end-diastolic pressure with a R<sup>2</sup> of 0.955. This novel ML algorithm could assist clinicians in the care of HF patients.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1307-1315"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11634911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626848","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
TMAO Impairs Mouse Aortic Vasodilation by Inhibiting TRPV4 Channels in Endothelial Cells. TMAO 通过抑制内皮细胞中的 TRPV4 通道损害小鼠主动脉血管舒张功能
IF 2.4 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-09 DOI: 10.1007/s12265-024-10543-5
Ning Zhang, Liangju Liu, Xiaowang Lv, Yixuan Wang, Wei Zhang, Xin Wen, Fan Yu, Tingting Zhou
{"title":"TMAO Impairs Mouse Aortic Vasodilation by Inhibiting TRPV4 Channels in Endothelial Cells.","authors":"Ning Zhang, Liangju Liu, Xiaowang Lv, Yixuan Wang, Wei Zhang, Xin Wen, Fan Yu, Tingting Zhou","doi":"10.1007/s12265-024-10543-5","DOIUrl":"10.1007/s12265-024-10543-5","url":null,"abstract":"<p><p>Trimethylamine oxide (TMAO) is an intestinal flora metabolite associated with risk of cardiovascular diseases. Transient receptor potential vanilloid 4 (TRPV4) is a Ca<sup>2+</sup>-permeable ion channel that is essential for vasodilation and endothelial function. Currently, there are few studies on the effect of TMAO on TRPV4 channels. In the present study, Ca<sup>2+</sup> imaging of vascular tissue showed that TMAO inhibited TRPV4-mediated Ca<sup>2+</sup> influx into aortic endothelial cells in a dose-dependent manner. Furthermore, a whole-cell patch clamp assay showed that TMAO blocked TRPV4-mediated cation currents. Notably, results of aortic vascular tension measurement showed that TMAO impaired endothelium-dependent vasodilation in mouse aortic vessels through the TRPV4-NO pathway. Our results indicated that TMAO inhibited Ca<sup>2+</sup> entry in endothelial cells and impaired vasodilation through the TRPV4-NO pathway in mice. These results provide scientific evidence for novel pathogenic mechanisms underlying the role of TMAO in cardiovascular disease.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1415-1426"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558846","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
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信