Cardiovascular Therapeutics最新文献

{"title":"Prodrug Strategies in Atherosclerosis: Targeted Delivery and Therapeutic Advances","authors":"Elaheh Mirhadi,&nbsp;Wael Almahmeed,&nbsp;Prashant Kesharwani,&nbsp;Amirhossein Sahebkar","doi":"10.1155/cdr/5159097","DOIUrl":"https://doi.org/10.1155/cdr/5159097","url":null,"abstract":"<p>Atherosclerosis is an advancing and complex vascular condition primarily associated with sustained inflammatory responses, oxidative imbalance, and disruptions in lipid homeostasis. These pathological features render it a major contributor to the global burden of cardiovascular disease, encompassing both morbidity and mortality. Traditional treatment modalities, including statins, angiotensin-converting enzyme inhibitors, PCSK9 inhibitors and surgical procedures, frequently encounter limitations due to inefficient pharmacokinetic profiles, insufficient targeting of pathological sites and widespread adverse effects. To address these therapeutic shortcomings, prodrug and nano-prodrug technologies have gained recognition as innovative systems capable of enabling site-specific and stimuli-activated therapeutic delivery in atherosclerotic disease management. This review discusses ROS-responsive prodrugs, biomimetic nano-prodrug platforms, and multifunctional theranostic nanotechnologies as alternative approaches for advanced atherosclerosis treatment. These systems enable targeted drug activation in oxidative plaque environments, improve pharmacokinetics, and enhance lesion-specific delivery via mechanisms such as VCAM-1 targeting, integrins, and cell membrane cloaking. Notably, in preclinical models nano-prodrugs have been reported to produce combined therapeutic effects by modulating lipid metabolism, reducing inflammation, and preventing foam cell formation, whereas theranostic platforms have enabled real-time monitoring of treatment response in animals. No nano-prodrug platform for atherosclerosis has yet been evaluated in humans. Despite progress, key barriers to clinical translation remain, including poor scalability and reproducibility of nanomaterials, patient variability in plaque biology, limited long-term safety data, and regulatory challenges for complex nanosystems. Future advances will require biomarker-guided patient selection, robust clinical validation, multistimuli-responsive designs, and well-defined regulatory standards. Overcoming these issues is vital for integrating nano-prodrug technologies into precision atherosclerosis therapy.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5159097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation Between Apolipoprotein B and Severity of Coronary Artery Stenosis in Individuals Aged 45 and Above: A Cross-Sectional Study","authors":"Dingchao Lv,&nbsp;Mao Ye,&nbsp;He Huang,&nbsp;Suqi Lv,&nbsp;Chen Li,&nbsp;Xiaolan Wang,&nbsp;Bin Yang","doi":"10.1155/cdr/2249959","DOIUrl":"10.1155/cdr/2249959","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Apolipoprotein B (ApoB) is widely recognized as a biomarker significantly associated with cardiovascular risk. However, the correlation between ApoB and the severity of coronary artery anatomical stenosis (Gensini score) in individuals aged 45 and above has not been fully studied.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A cross-sectional retrospective analysis was conducted, involving 818 patients who underwent coronary angiography. Fasting blood samples were collected to measure lipid parameters, including ApoB. The severity of coronary artery stenosis was assessed using the Gensini score, and patients were divided into two groups based on the median cut-off (&lt;36 vs. ≥ 36). A multivariate regression model was used to evaluate the association between ApoB and the severity of stenosis after adjusting for potential confounding factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared to the mild stenosis group (Gensini score &lt; 36), the moderate-to-severe stenosis group (score ≥ 36) had significantly higher levels of ApoB (1.0 ± 0.3 vs. 0.9 ± 0.3 g/L) and LDL-c (<i>p</i> &lt; 0.05), while HDL-c and ApoA levels were lower (<i>p</i> &lt; 0.001). Multivariate regression analysis indicated that ApoB was independently associated with moderate-to-severe coronary stenosis (<i>β</i> = 46.1, 95% CI: 31.3–61.0 <i>p</i> &lt; 0.001). Sensitivity analysis using continuous Gensini score confirmed the association (<i>β</i> = 22.57, 95% CI: 13.67–31.47, <i>p</i> &lt; 0.0001). Dose–response analysis revealed that higher ApoB tertiles were associated with progressively higher Gensini scores (<i>P</i> for trend = 0.001). Stratified analysis revealed a consistent positive correlation between ApoB and Gensini scores across all clinical subgroups (all <i>p</i> &lt; 0.05), with no significant interactions detected (all <i>P</i> for interaction &gt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>ApoB levels are significantly positively correlated with the severity of coronary artery stenosis in the population aged ≥ 45 years, indicating its potential clinical application value in evaluation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13443114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the Correlation Between Helper T-Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization Study","authors":"Jiahui Li,&nbsp;Yafen Yang,&nbsp;Hongxuan Fan,&nbsp;Zhuolin Huang,&nbsp;Yalin Yuan,&nbsp;Rui Bai,&nbsp;Xin Wang,&nbsp;Bin Liang","doi":"10.1155/cdr/4440768","DOIUrl":"10.1155/cdr/4440768","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Atrial fibrillation (AF) is the predominant arrhythmia. Growing evidence indicates that immunological diseases may play a role in its development. This study combined observational and genetic analyses to investigate how T-lymphocyte subsets and immunomodulatory drug targets influenced AF risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>This study retrospectively analyzed T lymphocyte subsets in 302 AF patients and 183 healthy controls. After balancing covariates via 1:1 propensity score matching, multivariate regression revealed AF patients had significantly higher absolute counts of Th1 and Th17 cells, and higher Th1/Th2 and Th17/Treg ratios (<i>p</i> &lt; 0.05). A subsequent two-sample Mendelian randomization (MR) analysis, which assessed 731 immune traits and included drug-target MR, established causal relationships. It showed that increased counts of CD4⁺CD8dim T cells (OR = 1.03, <i>p</i> = 0.002) and IgD⁻CD38dim B cells (OR = 1.06, <i>p</i> = 0.0003) elevated AF risk. Furthermore, IL-6R-mediated CRP elevation increased AF risk (OR = 1.33, <i>p</i> = 5.18E-7), whereas higher IL-18 gene expression was protective (OR = 0.95, <i>p</i> = 0.036).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Immune dysfunction, especially T lymphocyte subsets, is a risk factor for the development of AF. The IL-6R signaling pathway may be a potential target for AF prevention, whereas the use of IL-18 inhibitors may increase the risk of AF.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13438868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of Magnesium Status on the Association of Tobacco Exposure With Depression in Old Patients With Heart Failure: A Cross-Sectional Study of the NHANES Database","authors":"Yunyu Liang,&nbsp;Hua Jiang,&nbsp;Yan Zhong,&nbsp;Sijie Qiu,&nbsp;Xinmei Li,&nbsp;Pingchang Xie","doi":"10.1155/cdr/3372455","DOIUrl":"10.1155/cdr/3372455","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>The aim of this study is to examine the effect of magnesium depletion score (MDS) on the relationship between tobacco exposure and depression in older patients with heart failure (HF).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data from the National Health and Nutrition Examination Surveys (NHANES, 2005–2018) were analyzed in this cross-sectional study. Weighted logistic regression models were used to assess associations between MDS, tobacco exposure, and depression. Propensity score matching (PSM) was applied to minimize potential confounding.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 554 eligible participants, 166 presented with depression. After covariate adjustment, quitting smoking (robustness OR = 2.179, 95% CI: 1.190–3.685), current smoking (robustness OR = 1.941, 95% CI: 0.904–3.770), and serum cotinine ≥3 ng/mL (robustness OR = 1.968, 95% CI: 0.986–3.590) were significantly associated with increased depression risk. After PSM, quitting smoking (OR = 2.16, 95% CI: 1.13–4.12) and cotinine ≥3 ng/mL (OR = 2.47, 95% CI: 1.06–5.75) remained significantly associated with depression. Compared with MDS ≤ 2 combined with no smoking, MDS ≤ 2 combined with quitting smoking (robustness OR = 2.375, 95% CI: 1.076–4.739) and MDS &gt; 2 combined with quitting smoking (robustness OR = 3.142, 95% CI: 1.413–5.824) or currently smoking (robustness OR = 5.608, 95% CI: 1.790–13.661) were all linked to higher odds of depression. A significant multiplicative interaction between MDS and smoking was observed with <i>p</i> &lt; 0.001. Also, MDS &gt; 2 combined with serum cotinine ≥3 ng/mL was associated with higher odds of depression compared with MDS ≤ 2 combined with serum cotinine &lt; 0.05 ng/mL (robustness OR = 5.258, 95% CI: 1.869–11.546).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>MDS appears a possible interaction on the association between self-reported tobacco exposure and depression. Whether maintaining adequate magnesium status can help reduce depression risk in HF patients needs further validation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13382352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnetocardiography for Exploratory Risk Stratification in Patients With Three-Vessel Coronary Artery Disease: A Single-Center Prospective Cohort Study","authors":"Ziyu An,&nbsp;Shipan Wang,&nbsp;Min Zhang,&nbsp;Mingduo Zhang,&nbsp;Lanxin Feng,&nbsp;Shuwen Yang,&nbsp;Qi Zhou,&nbsp;Haiyang Hu,&nbsp;Chenchen Tu,&nbsp;Hongjia Zhang,&nbsp;Xiantao Song","doi":"10.1155/cdr/5552371","DOIUrl":"https://doi.org/10.1155/cdr/5552371","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Aims</h3>\u0000 \u0000 <p>Patients with three-vessel coronary artery disease (3V-CAD) remain at heterogeneous risk for major adverse cardiovascular and cerebrovascular events (MACCE) after revascularization. Magnetocardiography (MCG) is a noncontact and radiation-free technique that may capture electrophysiological abnormalities not reflected by anatomical risk scores. This study evaluated the exploratory prognostic value of MCG-derived parameters in patients with 3V-CAD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This single-center prospective cohort study included 544 patients with 3V-CAD who underwent coronary revascularization. MCG recordings were obtained before revascularization using a 36-channel optically pumped magnetometer-based system. The primary endpoint was MACCE, defined as cardiac death, stroke, myocardial infarction, or unplanned revascularization. Cox regression models were constructed using clinical variables, SYNTAX score, and an MCG composite variable. Model performance was assessed using discrimination, calibration, decision curve analysis, and bootstrap internal validation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>During a median follow-up of 725 days, 37 patients (6.8%) experienced MACCE. The SYNTAX score was independently associated with MACCE after adjustment for clinical variables and MCG score (hazard ratio [HR], 1.08; 95% confidence interval [CI], 1.04–1.12; <i>p</i> &lt; 0.001). The MCG composite variable was also associated with MACCE after adjustment for clinical variables and SYNTAX score (HR, 2.74; 95% CI, 1.57–4.79; <i>p</i> &lt; 0.001). Model discrimination increased from 0.596 for clinical variables alone to 0.682 after adding SYNTAX score and to 0.727 after adding MCG. However, the improvement from the clinical + SYNTAX model to the MCG-added model was not statistically significant (<i>p</i> = 0.17). Bootstrap validation showed an optimism-corrected <i>C</i>-index of 0.672.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>MCG-derived parameters were associated with MACCE and may provide complementary electrophysiological information for exploratory risk stratification in patients with 3V-CAD after revascularization. Larger multicenter studies with external validation are needed to confirm its complementary prognostic value.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>Chinese Clinical Trial Registry identifier: ChiCTR2200066942</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5552371","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and Validation of a Nomogram for Estimating Stroke Risk in Nonvalvular Atrial Fibrillation Patients With Left Atrial Stiffness: A Single-Center Cross-Sectional Study","authors":"Decai Zeng,&nbsp;Xiangling Cao,&nbsp;Yongzhi Cai,&nbsp;Tongtong Huang,&nbsp;Shuai Chang,&nbsp;Bingling Wu,&nbsp;Ji Wu","doi":"10.1155/cdr/8877050","DOIUrl":"https://doi.org/10.1155/cdr/8877050","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Nonvalvular atrial fibrillation (NVAF) is a prevalent arrhythmia associated with an increased risk of ischemic stroke. This study is aimed at assessing the clinical significance of echocardiographic left atrial (LA) stiffness and developing a nomogram integrating clinical and echocardiographic parameters to evaluate individualized stroke risk in NVAF patients.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We enrolled 402 consecutive NVAF patients between January 2020 and March 2023. Clinical and echocardiographic data were collected, and patients were randomly assigned to training (&lt;i&gt;n&lt;/i&gt; = 281) and validation (&lt;i&gt;n&lt;/i&gt; = 121) datasets. Univariate and multivariate logistic regression identified independent stroke risk factors, which were used to construct a nomogram. Model performance was evaluated by receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis. The reclassification ability of the nomogram was assessed using integrated discrimination improvement (IDI) and net reclassification improvement (NRI).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Logistic regression identified LA stiffness, LA reservoir strain, hypertension, peripheral vascular disease, and anticoagulation as independent factors associated with stroke. The nomogram based on these factors showed excellent discrimination, with a C-statistic of 0.889 (0.847–0.924) in the training cohort and 0.880 (0.808–0.932) in the validation cohort. Model A (LA stiffness, LA reservoir strain, hypertension, peripheral vascular disease, and anticoagulation) provided better net reclassification and integrated discrimination than Model B (LA stiffness, LA reservoir strain, hypertension, and peripheral vascular disease) despite both outperforming the CHA&lt;sub&gt;2&lt;/sub&gt;DS&lt;sub&gt;2&lt;/sub&gt;-VASc model. LA stiffness was inversely correlated with left atrial appendage (LAA) emptying (R = −0.52, &lt;i&gt;p&lt;/i&gt; &lt; 0.01) and filling velocities (R = −0.50, &lt;i&gt;p&lt;/i&gt; &lt; 0.01). Patients with LA thrombus or spontaneous echocardiographic contrast exhibited significantly higher LA stiffness (&lt;i&gt;p&lt;/i&gt; &lt; 0.05).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A nomogram incorporating LA stiffness, LASr, hypertension, and peripheral vascular disease can effectively identify the risk of stroke in NVAF patients. Additionally, a secondary model including anticoagulation showed further improved performance but requires prospective validation. Elevated LA stiffness might play a role in the development of stroke in NVAF by influencing LA appendage hemodynamics.&lt;/","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8877050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive Value of Serum Pepsinogen and Gastrin-17 in Patients With Acute Coronary Syndrome for Post-Percutaneous Coronary Intervention Oral Dual Antiplatelet Therapy-Associated Upper Gastrointestinal Bleeding","authors":"WanPing Yao,&nbsp;Chang Liu,&nbsp;ZiYi Fang,&nbsp;ShanShan Li,&nbsp;Lu Hong Xu,&nbsp;WenHao Qian,&nbsp;Fangfang Li,&nbsp;Jing Zong","doi":"10.1155/cdr/8095418","DOIUrl":"10.1155/cdr/8095418","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Gastrin-17 (G-17) and serum pepsinogen (PG) are indicators that reflect the structure and function of the stomach mucosa. Although they have been linked to upper gastrointestinal bleeding (UGIB) in peptic ulcer disease, it is unknown how they relate to the risk of UGIB in patients with acute coronary syndrome (ACS) after dual antiplatelet treatment (DAPT) following percutaneous coronary intervention (PCI).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Objective&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This single-center, retrospective study aims to evaluate whether PG and G-17 as gastric mucosal assessment markers, are potentially associated with UGIB during DAPT following PCI in patients with ACS.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This study employed a retrospective analysis design and included 334 patients with ACS (2021–2023) from Xuzhou Medical University Affiliated Hospital, divided into UGIB group (69 patients) and non-UGIB group (265 patients). Clinical and laboratory data were collected. Multivariate logistic regression and ROC curve analysis were used to evaluate the associations of G-17, PRECISE-DAPT scores, ACS subtype, and P&lt;sub&gt;2&lt;/sub&gt;Y&lt;sub&gt;12&lt;/sub&gt; receptor antagonist used for UGIB after DAPT.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Compared with the non-UGIB group, G-17 levels and PRECISE-DAPT scores in the UGIB group were markedly higher, and ticagrelor was prescribed more commonly (&lt;i&gt;p&lt;/i&gt; &lt; 0.001). The area under the curve (AUC) of G-17, PRECISE-DAPT scores alone, and in combination were 0.734, 0.794, and 0.844, respectively; the AUC further increased to 0.878 after incorporating ticagrelor exposure, indicating that the combined assessment with ticagrelor exposure has superior exploratory value in identifying high-risk patients with UGIB (&lt;i&gt;p&lt;/i&gt; &lt; 0.05). Furthermore, the combined use of PPIs during DAPT reduced the incidence of UGIB (34.78% vs. 65.22%, &lt;i&gt;p&lt;/i&gt; &lt; 0.05), which serves as an important interfering factor for G-17 assessment.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Higher G-17 levels and PRECISE-DAPT scores were associated with UGIB during DAPT after PCI. Combined assessment with ticagrelor exposure showed exploratory value for identifying patients at higher bleeding risk, although PPIs use influenced model performance. Given the retrospective single-center design and limited sample size, these findings remain preliminary and require prospective multicenter validation.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 ","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8095418","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148429856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Asprosin Protects H9C2 Cells From Ferroptosis Following Hypoxia/Reoxygenation by Promoting Mitophagy”","authors":"","doi":"10.1155/cdr/9810149","DOIUrl":"https://doi.org/10.1155/cdr/9810149","url":null,"abstract":"<p>X. Wang, X. Zhang, H. Tang, et al., “Asprosin Protects H9C2 Cells From Ferroptosis Following Hypoxia/Reoxygenation by Promoting Mitophagy,” <i>Cardiovascular Therapeutics</i> 2026 (2026): 8401037, https://doi.org/10.1155/cdr/8401037</p><p>In this above article, there was an error in the affiliation. The correct affiliation list and author affiliations are shown below.</p><p>Xiangkun Wang¹, Xiaoyu Zhang², Huaiguang Tang¹, Xiaojuan Su³, Shutong Ding³, Xuelian Li⁴, and Bingong Li⁵</p><p>¹Department of Cardiology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China</p><p>²Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang Province, China</p><p>³School of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, China</p><p>⁴Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China</p><p>⁵Department of Cardiology, Qingdao Hospital of Rehabilitation University, East Hospital of Qingdao Municipal Hospital, Qingdao, Shandong, China</p><p>We apologize for this error.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9810149","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148466928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basement Membrane–Related Genes C1QTNF3, PTGER2, CAMK2N1, PRSS36, and B3GNT7: Novel Biomarkers for Coronary Artery Disease","authors":"Zhao Dong,&nbsp;Yuyu Zhang,&nbsp;Zhuang Li,&nbsp;Haozhen Yu,&nbsp;Wei Ge","doi":"10.1155/cdr/5358909","DOIUrl":"10.1155/cdr/5358909","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Basement membrane–related genes (BMRGs) play a pivotal role in the pathogenesis of several diseases. However, their association with coronary artery disease (CAD) remains unexplored. Therefore, this investigation is designed to elucidate the involvement of BMRGs in CAD mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study incorporated CAD-related datasets (GSE113079 and GSE125856) and BMRGs. Initially, differentially expressed genes (DEGs) were identified between CAD and control (CTL) groups in GSE113079 and GSE125856. Subsequently, weighted gene coexpression network analysis (WGCNA) was carried out to identify key module genes associated with basement membranes. We then intersected the DEGs with the key module genes to obtain differentially expressed basement membrane–related genes (DE-BMRGs). Two machine learning algorithms were applied to recognize feature genes, and the intersection of these features yielded the key genes. Subsequently, immune analysis, regulatory network construction, nomogram development, and expression verification were executed based on key genes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Five key genes were identified: C1QTNF3, PTGER2, CAMK2N1, PRSS36, and B3GNT7. Among these, C1QTNF3 (AUC = 0.954), PTGER2 (AUC = 0.878), CAMK2N1 (AUC = 0.872), and B3GNT7 (AUC = 0.855) exhibited strong diagnostic potential in GSE113079, whereas PRSS36 showed more modest performance (AUC = 0.667). Moreover, 11 differences were observed in immune cell populations between the two groups (<i>p</i> &lt; 0.05), including CD8 T cells, and we constructed a TF-miRNA-gene network comprising 112 regulatory relationships, such as the regulation of C1QTNF3 by SMAD4 and hsa-miR-302a-3p. Additionally, the expression of these five key genes was consistently lower in the CAD group across GSE113079, GSE125856, and clinical patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study identified five key genes associated with the basement membrane (C1QTNF3, PTGER2, CAMK2N1, PRSS36, and B3GNT7) that offer valuable scientific insights into the mechanisms of CAD. These genes represent candidate noninvasive molecular markers requiring further validation for early diagnosis and serve as preliminary candidates for subsequent therapeutic target exploration.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5358909","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salvianolic Acid B Alleviates Atrial Fibrillation–Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway","authors":"Pengran Wang,&nbsp;Jianhua Ma,&nbsp;Jianlong Li,&nbsp;Shanshan Li,&nbsp;Yeran Zhu,&nbsp;Ruibin Li,&nbsp;Jidong Zhang","doi":"10.1155/cdr/5515602","DOIUrl":"10.1155/cdr/5515602","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Atrial fibrillation (AF), the most prevalent cardiac arrhythmia, is strongly associated with atrial fibrosis. Salvianolic acid B (Sal-B), a bioactive compound extracted from <i>Salvia miltiorrhiza</i>, demonstrates cardioprotective properties, though its specific role in AF remains to be elucidated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Transcriptome analysis of the GSE115574 dataset was performed to identify <i>COL1A2</i> as a differentially expressed gene in patients with AF. Molecular docking simulations were performed to evaluate the binding affinity between Sal-B and COL1A2. For in vitro experiments, an injury model was established in AC16 cardiomyocytes using Angiotensin II (Ang-II) treatment, followed by intervention with either Sal-B (80 <i>μ</i>g/mL) or <i>COL1A2</i> siRNA. Cellular viability, apoptosis, migration capacity, and fibrosis markers (COL1A1, <i>α</i>-SMA, and collagen III) were subsequently assessed. In vivo studies employed an ACh-CaCl₂–induced AF rat model, with cardiac function evaluated through electrocardiography (ECG) and echocardiography. Myocardial tissue damage was examined via hematoxylin–eosin (HE) staining and Masson′s trichrome staining. Western blot analysis was used to determine COL1A2 expression and PI3K-AKT pathway activity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p><i>COL1A2</i> expression was significantly upregulated in AF, and molecular docking demonstrated its strong binding affinity for Sal-B. Sal-B treatment rescued Ang-II–induced cardiomyocyte damage, reduced apoptosis, and suppressed fibrosis marker expression. In rat models, either Sal-B or si-<i>COL1A2</i> alone shortened the AF duration, improved cardiac function (attenuated the elevated <i>E</i>/<i>E</i>^′ ratio while restoring the ejection fraction), and reduced fibrosis and inflammation. The combined treatment synergistically restored sinus rhythm and normalized collagen deposition, suggesting a modulatory role of Sal-B in these processes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Sal-B alleviates AF in association with COL1A2 modulation and PI3K-AKT signaling pathway inhibition, which may contribute to reducing atrial fibrosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5515602","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}