Clinical and Experimental Hypertension最新文献

{"title":"Restoration of vascular dysfunction resulting from maternal high-fat diet via modulation of the NLRP3/IL-1β axis.","authors":"Yuxuan Xiao, Xianru Bi, Rongjie Zhang, Yu Li, Wei Sun, Yingxue Hao","doi":"10.1080/10641963.2024.2440342","DOIUrl":"https://doi.org/10.1080/10641963.2024.2440342","url":null,"abstract":"<p><p>This study investigated the impact of maternal high-fat diet on vascular function and endothelial homeostasis in offspring. We found that offspring exposed to maternal high-fat diet exhibited elevated blood pressure, impaired abdominal aortic vascular function, and endothelial homeostasis imbalance. These changes were accompanied by increased levels of reactive oxygen species (ROS) and upregulation of pro-inflammatory cytokines (including IL-1β, TNF-α, IL-6, and IL-10). Treatment with NLRP3 or IL-1β inhibitors prevented the deterioration in vascular function, reduced endothelial NO production, and inflammation induced by maternal high-fat diet exposure compared to the control group. The findings suggest that during pregnancy, mitigating the vascular impairments in offspring induced by maternal high-fat diet can be achieved by inhibiting the NLRP3/IL-1β pathway.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2440342"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-based analyses of contributing factors for the development of hypertension: a comparative study.","authors":"Marenao Tanaka, Yukinori Akiyama, Kazuma Mori, Itaru Hosaka, Keisuke Endo, Toshifumi Ogawa, Tatsuya Sato, Toru Suzuki, Toshiyuki Yano, Hirofumi Ohnishi, Nagisa Hanawa, Masato Furuhashi","doi":"10.1080/10641963.2025.2449613","DOIUrl":"https://doi.org/10.1080/10641963.2025.2449613","url":null,"abstract":"<p><strong>Objectives: </strong>Sufficient attention has not been given to machine learning (ML) models using longitudinal data for investigating important predictors of new onset of hypertension. We investigated the predictive ability of several ML models for the development of hypertension.</p><p><strong>Methods: </strong>A total of 15 965 Japanese participants (men/women: 9,466/6,499, mean age: 45 years) who received annual health examinations were randomly divided into a training group (70%, <i>n</i> = 11,175) and a test group (30%, <i>n</i> = 4,790). The predictive abilities of 58 candidates including fatty liver index (FLI), which is calculated by using body mass index, waist circumference and levels of γ-glutamyl transferase and triglycerides, were investigated by statistics analogous to the area under the curve (AUC) in receiver operating characteristic curve analyses using ML models including logistic regression, random forest, naïve Bayes, extreme gradient boosting and artificial neural network.</p><p><strong>Results: </strong>During a 10-year period (mean period: 6.1 years), 2,132 subjects (19.1%) in the training group and 917 subjects (19.1%) in the test group had new onset of hypertension. Among the 58 parameters, systolic blood pressure, age and FLI were identified as important candidates by random forest feature selection with 10-fold cross-validation. The AUCs of ML models were 0.765-0.825, and discriminatory capacity was significantly improved in the artificial neural network model compared to that in the logistic regression model.</p><p><strong>Conclusions: </strong>The development of hypertension can be simply and accurately predicted by each ML model using systolic blood pressure, age and FLI as selected features. By building multiple ML models, more practical prediction might be possible.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2449613"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Chicoric acid</i> advanced PAQR3 ubiquitination to ameliorate ferroptosis in diabetes nephropathy through the relieving of the interaction between PAQR3 and P110α pathway.","authors":"Weiwei Zhang, Yong Liu, Jiajun Zhou, Teng Qiu, Haitang Xie, Zhichen Pu","doi":"10.1080/10641963.2024.2326021","DOIUrl":"10.1080/10641963.2024.2326021","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to examine the impact of CA on DN and elucidate its underlying molecular mechanisms of inflammation.</p><p><strong>Methods: </strong>We fed C57BL/6 mice injected with streptozotocin to induce diabetes. In addition, we stimulated NRK-52E cells with 20 mmol/L d-glucose to mimic the diabetic condition.</p><p><strong>Results: </strong>Our findings demonstrated that CA effectively reduced blood glucose levels, and improved DN in mice models. Additionally, CA reduced kidney injury and inflammation in both mice models and in vitro models. CA decreased high glucose-induced ferroptosis of NRK-52E cells by inducing GSH/GPX4 axis. Conversely, the ferroptosis activator or the PI3K inhibitor reversed positive effects of CA on DN in both mice and in vitro models. CA suppressed PAQR3 expression in DN models to promote PI3K/AKT activity. The PAQR3 activator reduced the positive effects of CA on DN in vitro models. Moreover, CA directly targeted the PAQR3 protein to enhance the ubiquitination of the PAQR3 protein.</p><p><strong>Conclusion: </strong>Overall, our study has uncovered that CA promotes the ubiquitination of PAQR3, leading to the attenuation of ferroptosis in DN. This effect is achieved through the activation of the PI3K/AKT signaling pathways by disrupting the interaction between PAQR3 and the P110α pathway. These findings highlight the potential of CA as a viable therapeutic option for the prevention of DN and other forms of diabetes.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2326021"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the current status and associated risk factors of cognitive function in Tibetan hypertensive patients at various altitudes.","authors":"Long Yin, Xiaoming Zhang, Huijuan Zhang, Ruizhen Li, Jing Zeng, Kaixuan Dong, Yi Wang, Xinghui Li","doi":"10.1080/10641963.2024.2393331","DOIUrl":"https://doi.org/10.1080/10641963.2024.2393331","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to explore the current cognitive status and identify risk factors associated with cognitive function in Tibetan hypertensive patients living at various altitudes.</p><p><strong>Methods: </strong>The Simple Mental Status Scale (MMSE) was used to evaluate the cognitive function of 611 Tibetan hypertensive patients at various altitudes in Gannan Tibetan Autonomous Prefecture. Afterward, we conducted an analysis to identify the factors influencing their cognitive function.</p><p><strong>Results: </strong>The study found that the prevalence of cognitive dysfunction was 22.3%, with a higher incidence at high altitude (group D 29.0%) compared to low altitude (group A 16.0%). The study conducted a binary logistic regression analysis to identify the risk factors for cognitive dysfunction. The analysis revealed that altitude, age, body mass index, marital status, education, income level, and blood pressure control level were all significant risk factors. After controlling for age, body mass index, marital status, educational level, income level, and blood pressure control level, the risk of developing cognitive dysfunction was 2.773 times higher (<i>p</i> < .05) for individuals in group C at high altitude and 2.381 times higher (<i>p</i> < .05) for individuals in group D at high altitude compared to those in group A at low altitude.</p><p><strong>Conclusions: </strong>Altitude plays a role in the development of cognitive dysfunction in hypertensive patients. Tibetan hypertensive patients living at high altitudes may be at a higher risk of cognitive dysfunction compared to those living at lower altitudes. Therefore, interventions should be targeted to prevent or mitigate potential cognitive impairment.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2393331"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research hotspots and trends regarding microRNAs in hypertension: a bibliometric analysis.","authors":"Yu Sun, Qingxin Shang","doi":"10.1080/10641963.2024.2304017","DOIUrl":"10.1080/10641963.2024.2304017","url":null,"abstract":"<p><p>To investigate the research levels, hotspots, and development trends regarding microRNAs in hypertension, this study conducted a visual analysis of studies on miRNA in hypertension based on the Web of Science core collection database using CiteSpace and VOSviewer analysis software along with literature from 2005-2023 as information data. Using citation frequency, centrality, and starting year as metrics, this study analyzed the research objects. It revealed the main research bodies and hotspots and evaluated the sources of literature and the distribution of knowledge from journals and authors. Finally, the potential research directions for miRNAs in hypertension are discussed. The results showed that the research field is in a period of vigorous development, and scholars worldwide have shown strong interest in this research field. A comprehensive summary and analysis of the current research status and application trends will prove beneficial for the advancement of this field.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2304017"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139478216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uric acid mediates kidney tubular inflammation through the LDHA/ROS/NLRP3 pathway.","authors":"Jun Ouyang, Hui Wang, Yumei Gan, Jiangnan Huang","doi":"10.1080/10641963.2024.2424834","DOIUrl":"10.1080/10641963.2024.2424834","url":null,"abstract":"<p><strong>Purpose: </strong>Hyperuricemia (HUA) is an important factor leading to chronic kidney disease (CKD). The kidney tubular inflammatory response is activated in HUA. This study aimed to investigate whether lactate dehydrogenase A (LDHA) is involved in mediating uric acid-induced kidney tubular inflammatory response.</p><p><strong>Methods: </strong>In vivo, an HUA mouse model was established by continuous intraperitoneal injection of potassium oxonate (PO) for one week. A total of 18 C57BL/6J male adult mice were divided into three groups: control group, HUA group, and HUA+oxamate group, with six mice in each group. Oxamate was intraperitoneally injected into the mice one hour after PO injection. In vitro, an HUA model was simulated by stimulating HK-2 cells with uric acid. Oxamate and tempol inhibited LDHA and reactive oxygen species (ROS) in HK-2 cells.</p><p><strong>Results: </strong>In HUA mice, blood uric acid levels were significantly elevated. LDHA in kidney tubular cells was significantly increased in both in vivo and in vitro HUA models, accompanied by an increase in kidney tubular inflammation and ROS. Mechanistically, LDHA mediates uric acid-induced inflammation to kidney tubular cells through the ROS/NLRP3 pathway. Pharmacologic inhibition of LDHA or ROS in kidney tubular cells can significantly ameliorate inflammation response caused by uric acid.</p><p><strong>Conclusions: </strong>LDHA in kidney tubular cells significantly was increased in HUA models. LDHA mediates kidney inflammation response induced by uric acid through the ROS/NLRP3 pathway. This study may provide a new intervention target for preventing kidney tubular inflammation caused by uric acid.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2424834"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT5-mediated PRKAA2 succinylation ameliorates apoptosis of human placental trophoblasts in hypertensive disorder complicating pregnancy.","authors":"Feifei Ren, Mo Yang, Guangman Liu, Yuyan Qi, Aijie Li, Jia Li, Lili Zheng","doi":"10.1080/10641963.2024.2358030","DOIUrl":"10.1080/10641963.2024.2358030","url":null,"abstract":"<p><strong>Purpose: </strong>Hypertensive disorder complicating pregnancy (HDCP) is a serious clinical disorder syndrome during pregnancy. This study aims at finding novel targets for HDCP therapy.</p><p><strong>Methods: </strong>HDCP-related mRNAs were firstly screened out and subjected to gene enrichment analysis. We chose protein kinase AMP-activated catalytic subunit alpha 2 (PRKAA2) as the research object. Thirty-nine HDCP patients at 32 to 40 weeks of gestation were selected as the HDCP group, and 39 normal controls who received cesarean section delivery at 37-42 weeks of pregnancy were enrolled in this study. Chorionic villi samples were collected within 30 min of delivery. The apoptosis of isolated placental trophoblasts was monitored to investigate the regulatory role of PRKAA2.</p><p><strong>Results: </strong>PRKAA2 expression was further proven to be enhanced in the placental tissues of HDCP patients compared with that of normal puerpera. Subsequently, the results of flow cytometry analysis and western blot indicated that PRKAA2 overexpression accelerated primary placental cell apoptosis, while its knockdown attenuated cell apoptosis. Mechanistically, we determined that the level of PRKAA2 succinylation was elevated in the placental tissue of HDCP patients. Through in vitro succinylation assay and mutagenesis, we confirmed that sirtuin 5 (SIRT5) interacts with PRKAA2 at K69 and K260 to induce PRKAA2 desuccinylation. SIRT5 regulated primary HDCP cell apoptosis through PRKAA2. Finally, the animal study revealed that PRKAA2 elevates the systolic blood pressure of HDCP rat model.</p><p><strong>Conclusion: </strong>Our findings indicated that SIRT5-mediated PRKAA2 succinylation modulates placental cell apoptosis in HDCP, suggesting that PRKAA2 is a potential therapeutic target for HDCP treatment.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2358030"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing the aldosterone-to-renin ratio cut-off for screening primary aldosteronism based on cardiovascular risk: a collaborative study.","authors":"Chunxue He, Ruolin Li, Jun Yang, Hang Shen, Yue Wang, Xiangjun Chen, Wenjin Luo, Qinglian Zeng, Linqiang Ma, Ying Song, Qingfeng Cheng, Zhihong Wang, Fei-Fei Wu, Qifu Li, Shumin Yang, Jinbo Hu","doi":"10.1080/10641963.2023.2301571","DOIUrl":"10.1080/10641963.2023.2301571","url":null,"abstract":"<p><strong>Objectives: </strong>Aldosterone-to-renin ratio (ARR) based screening is the first step in the diagnosis of primary aldosteronism (PA). However, the guideline-recommended ARR cutoff covers a wide range, from the equivalent of 1.3 to 4.9 ng·dl^-1/mIU∙l^-1. We aimed to optimize the ARR cutoff for PA screening based on the risk of cardiovascular diseases (CVD).</p><p><strong>Methods: </strong>Longitudinally, we included hypertensive participants from the Framingham Offspring Study (FOS) who attended the sixth examination cycle and followed up until 2014. At baseline (1995-1998), we used circulating concentrations of aldosterone and renin to calculate ARR (unit: ng·dl^-1/mIU∙l^-1) among 1,433 subjects who were free of CVD. We used spline regression to calculate the ARR threshold based on the incident CVD. We used cross-sectional data from the Chongqing Primary Aldosteronism Study (CONPASS) to explore whether the ARR cutoff selected from FOS is applicable to PA screening.</p><p><strong>Results: </strong>In FOS, CVD risk increased with an increasing ARR until a peak of ARR 1.0, followed by a plateau in CVD risk (hazard ratio 1.49, 95%CI 1.19-1.86). In CONPASS, when compared to essential hypertension with ARR < 1.0, PA with ARR ≥ 1.0 carried a higher CVD risk (odds ratio 2.24, 95%CI 1.41-3.55), while essential hypertension with ARR ≥ 1.0 had an unchanged CVD risk (1.02, 0.62-1.68). Setting ARR cutoff at 2.4 ~ 4.9, 10% ~30% of PA subjects would be unrecognized although they carried a 2.45 ~ 2.58-fold higher CVD risk than essential hypertension.</p><p><strong>Conclusions: </strong>The CVD risk-based optimal ARR cutoff is 1.0 ng·dl^-1/mIU∙l^-1 for PA screening. The current guideline-recommended ARR cutoff may miss patients with PA and high CVD risk.</p><p><strong>Clinical trial registration: </strong>ClinicalTrials.gov (NCT03224312).</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2301571"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139545995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal relationship between gut microbiota, plasma metabolites, inflammatory cytokines and abdominal aortic aneurysm: a Mendelian randomization study.","authors":"Chaozhong Li, Zhengqing Liu, Siqian Yang, Wanrong Li, Bo Liang, Haoyu Chen, Yujia Ye, Fang Wang, Xiaoqing Liu, Yongliang Jiang, Haiying Wu, Yunzhu Peng, Zhaohui Meng","doi":"10.1080/10641963.2024.2390419","DOIUrl":"https://doi.org/10.1080/10641963.2024.2390419","url":null,"abstract":"<p><strong>Background: </strong>Complex interconnections are evident among gut microbiota, circulating metabolites, inflammatory cytokines, and the pathogenesis of abdominal aortic aneurysms (AAA), with the causal dynamics yet to be comprehensively elucidated. The primary objective of this study was to elucidate the potential causal relationships involving gut microbiota-mediated plasma metabolites, inflammatory cytokines, and AAA.</p><p><strong>Methods: </strong>We utilized data from genome-wide association studies predominantly comprising individuals of European ancestry, encompassing four major gut microbiota signatures, 233 plasma metabolite signatures (<i>N</i> = 136,016), 91 inflammatory cytokine signatures (<i>N</i> = 14,824), and AAA signatures (<i>N</i> = 1,458,875). Mendelian randomization (MR), employed in a two-sample format, was utilized as a tool to investigate the potential causal pathways from gut microbiota to the development of AAA. Additionally, a two-step MR approach was employed to dissect the impact of plasma metabolites and inflammatory cytokines on the relationship between gut microbiota and AAA and to ascertain the mediated fractions.</p><p><strong>Results: </strong>Our findings indicate that five phylum or family-identical bacteria, 175 plasma metabolites, and seven inflammatory factors are causally associated with AAA. Among them, five bacterial species from the same phylum or family, identified from different GWAS data, were strongly associated with AAA. Of these, two exhibited negative causality and three exhibited positive causality. We found that the phylum <i>Firmicutes</i> and the families <i>Oscillospiraceae</i> might reduce the risk of AAA, whereas the families <i>Prevotellaceae</i>, <i>Sutterellaceae</i>, and <i>Aminobacteriaceae</i> might increase the risk of AAA. Further screening indicated that phylum <i>Firmicutes</i> id.1672 (GCST90017114) may confer a protective effect against AAA by reducing triglyceride levels in medium/small high-density lipoprotein (HDL).</p><p><strong>Conclusion: </strong>MR analysis has delineated a causal pathway from gut microbiota, through plasma circulating metabolites and inflammatory cytokines, to the pathogenesis of AAA. The role of intestinal flora and certain biomarkers may provide a reference for the diagnosis of AAA, and contribute to the prevention, diagnosis, and treatment of AAA disease.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2390419"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141970775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration and validation of signature genes and immune associations in septic cardiomyopathy.","authors":"Zhengbo Zhao, Xiaojing Wang, Fangyan Tan, Han Liu, Wan Chen, Jing Wang, Songbai Deng, Jianlin Du","doi":"10.1080/10641963.2024.2302570","DOIUrl":"https://doi.org/10.1080/10641963.2024.2302570","url":null,"abstract":"<p><p>An early and accurate diagnosis of septic cardiomyopathy is vital for improving the overall prognosis of sepsis. In our research, we aimed to identify signature genes and their immune connections in septic cardiomyopathy. By analyzing the mouse myocardial transcriptome from sepsis induced by cecum ligation and puncture (CLP), we identified four distinct k-means clusters. Further analysis of human myocardial datasets using Weighted Gene Co-expression Network Analysis (WGCNA) revealed a strong correlation between the MEturquoise module and septic cardiomyopathy (cor = 0.79, <i>p</i> < .001). Through the application of Cytoscape plug-in MCODE and comprehensive analysis, we pinpointed two signature genes, THBS1 and TIMP1. These genes demonstrated significant involvement in immune cell infiltration, as detected by CIBERSORT, and displayed promising prognostic potential as validated by external datasets. Our experimental validation confirmed the up-regulation of both THBS1 and TIMP1 in septic murine hearts, underscoring their positive association with septic cardiomyopathy.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2302570"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139569975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}