Cardiovascular Therapeutics最新文献

{"title":"Impella Versus Selective Biatrial Canulation for Left Ventricular Unloading During Extracorporeal Membrane Oxygenation","authors":"Mouhamed Djahoum Moussa,&nbsp;Jean Roux,&nbsp;Marie Jungling,&nbsp;Nassima Ramdane,&nbsp;Valentin Loobuyck,&nbsp;Benoit Brassart,&nbsp;Natacha Rousse,&nbsp;Céline Dupré,&nbsp;Agnès Mugnier,&nbsp;Abdelilah Khalipha,&nbsp;Adham Sameer A. Bardeesi,&nbsp;Oliver Lukowiak,&nbsp;Loïc Lefebvre,&nbsp;Francis Juthier,&nbsp;Emmanuel Robin,&nbsp;Julien Labreuche,&nbsp;Lise Thellier,&nbsp;André Vincentelli","doi":"10.1155/cdr/3669575","DOIUrl":"10.1155/cdr/3669575","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Comparisons of preload unloading techniques for left ventricle overdistension during venoarterial (VA) extracorporeal membrane oxygenation (ECMO) support are scarce. We compared outcomes in patients with left ventricular distension treated with cannulated percutaneous atrioseptostomy combined with ECMO—specified as selective biatrial extracorporeal membrane oxygenation (SBA-ECMO)—versus those treated with Impella CP/5.0 in combination with ECMO (ECPELLA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Consecutive adult patients who received VA-ECMO and underwent additional left ventricle unloading between January 2014 and March 2023 were studied. The primary endpoint was the number of ventilation-free days. The secondary endpoints were serious bleeding, blood product consumption, thrombotic complications, and 28-day mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We included 57 patients, 27 of whom received SBA-ECMO and 30 of whom received ECPELLA. The median number of ventilation-free days was 10 days (0–23) with SBA-ECMO and 5 days (0–23) with the ECPELLA (<i>p</i> = 0.61). According to the multivariable analyses, SBA-ECMO was associated with a lower risk of serious bleeding (HR 0.31 [95% CI 0.12–0.80]) and less blood product consumption (RR 0.57 [95% CI 0.36–0.90]) than ECPELLA. Thrombotic complications and 28-day mortality were similar between the groups before and after multivariable analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In patients with left ventricle congestion during VA-ECMO support, left ventricle unloading with SBA-ECMO was associated with reduced serious bleeding and transfusions compared with ECPELLA, despite a similar number of ventilation-free days, thrombotic complications, and mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>ClinicalTrials.gov identifiers: NCT03431467 and NCT05577195</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156032","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":"Hypermetabolism and Lipid Alterations Postburn: A Cardiovascular Perspective","authors":"Mohammed AbuBaha,&nbsp;Ameer Awashra,&nbsp;Bara AbuBaha,&nbsp;Anwar Zahran,&nbsp;Mohammad Bdair,&nbsp;Dana Sandouka,&nbsp;Sarah Saife,&nbsp;Bara Sawalmeh,&nbsp;Amr Awad,&nbsp;Abdalhakim Shubietah","doi":"10.1155/cdr/5983391","DOIUrl":"10.1155/cdr/5983391","url":null,"abstract":"<p>Severe thermal burns involving ≥ 20% of total body surface area (TBSA) initiate a distinct, prolonged physiological cascade extending well beyond the acute phase. This dysregulated response features chronic hypermetabolism, lipid remodeling, and sustained cardiovascular stress. While survival has improved with advances in acute care, the long-term cardiometabolic effects, particularly the link between lipid abnormalities and cardiovascular risk, remain underexplored. This review highlights the complex pathophysiology of burn-induced hypermetabolism, including elevated resting energy expenditure, catecholamine-driven lipolysis, mitochondrial uncoupling, and maladaptive adipose browning. Even in metabolically healthy individuals, these mechanisms promote atherogenic dyslipidemia, characterized by hepatic steatosis, elevated small-dense LDL, reduced HDL-C, and persistent hypertriglyceridemia. Emerging lipidomic and clinical data correlate these changes with increased Framingham risk scores, systemic inflammation, and TBSA extent. Simultaneously, cardiovascular vulnerability increases due to myocardial remodeling, autonomic dysfunction, and vascular impairment, particularly in young survivors with prolonged metabolic responses. Imaging and metabolomics reveal endothelial injury, subclinical cardiac dysfunction, and elevated arrhythmogenic risk persisting years after healing. We evaluate current interventions, <i>β</i>-blockers, omega-3 fatty acids, statins, anti-inflammatory agents, and structured rehabilitation, within a multimodal framework. Additionally, we identify critical gaps, including the need for precision metabolic modulation, omics-based monitoring, and tailored cardiovascular risk algorithms. Recognizing severe burns as systemic illnesses with delayed but measurable cardiovascular consequences requires a paradigm shift in long-term care. This review advocates for proactive, multidisciplinary cardiometabolic surveillance as an essential component of postburn recovery. This review follows the TITAN 2025 guideline for transparency in research and reporting.¹</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12878538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146141191","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":"Potential Diagnostic and Therapeutic Uses of DPT in Acute Type A Aortic Dissection","authors":"Ting Wei,&nbsp;Xiaopeng Yang,&nbsp;Chao Shi","doi":"10.1155/cdr/8896404","DOIUrl":"10.1155/cdr/8896404","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>Acute Type A aortic dissection (ATAAD) is a catastrophic cardiovascular emergency with high mortality and few treatment options. Diagnostic biomarkers or targeted treatments remain in the rudimentary stage, complicating early detection and intervention. The aim is to discover novel diagnostic and therapeutic biomarkers for ATAAD through integrated bioinformatics and experimental validation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Differentially expressed genes (DEGs) were identified using the “limma” package in R, applying the combined, normalized, and batch-effect-corrected microarray datasets GSE52093 and GSE98770. Functional enrichment analyses (GO and KEGG), protein–protein interaction (PPI) network construction, and weighted gene coexpression network analysis (WGCNA) were performed to identify key genes. Key genes were validated by qPCR, immunofluorescence, and functional assays in human aortic smooth muscle cells (HASMCs) and an independent dataset (GSE153434).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>There were 441 DEGs with 164 upregulated and 277 downregulated genes. These hub genes also overlapped with four key genes (DPT, ITGA5, HGF, and PLAUR) in the key WGCNA module. Of these, DPT was downregulated compared with ATAAD tissues. DPT knockdown induced HASMC migration and inhibited HASMC proliferation, as assessed by functional assays. The diagnostic potential of these genes, especially of DPT, was confirmed using ROC analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>DPT is a promising diagnostic and therapeutic biomarker for ATAAD. Downregulation may also disturb extracellular matrix homeostasis and smooth muscle cell function, leading to aortic wall instability. These findings provide a foundation for future research on DPT-targeted interventions for ATAAD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12880953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146141255","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":"Epiafzelechin, a Flavanol, Regulates Lipid Homeostasis Through Modulation of HMGCR, PCSK9, and PPAR-α: Mechanistic Insights and Therapeutic Implications","authors":"Saud O. Alshammari,&nbsp;Nazifa Shahzad,&nbsp;Muhammad Nasir Hayat Malik,&nbsp;Qamar A. Alshammari,&nbsp;Abdulkarim Alshammari,&nbsp;Bassam S. M. Al Kazman,&nbsp;Muhammad Atif,&nbsp;Gideon F. B. Solre","doi":"10.1155/cdr/9082023","DOIUrl":"10.1155/cdr/9082023","url":null,"abstract":"<p>Hyperlipidemia remains a leading modifiable risk factor for cardiovascular morbidity and mortality. Statins are considered the cornerstone of treatment; however, their adverse effects and limited efficacy in certain patient populations necessitate exploration of novel therapeutic avenues. Epiafzelechin (EZN), a flavanol with established antioxidant and anti-inflammatory properties, was investigated for its potential role in lipid metabolism using an integrative approach combining network pharmacology, molecular docking, and in vivo validation. Putative EZN targets were predicted through SuperPred, Way2Drug, and PharmMapper, and intersected with hyperlipidemia-related genes from GeneCards, DisGeNET, and CTD. Overlapping genes were subjected to protein–protein interaction (PPI) mapping, hub gene identification, and pathway enrichment analysis. Molecular docking was conducted to assess the binding affinity of EZN to lipid-regulating proteins. Therapeutic efficacy of EZN was also evaluated in a TWR-1339-induced hyperlipidemic rat model using biochemical assays and real-time PCR for gene expression profiling. A total of 105 genes were identified, involved in lipid transport, inflammatory signaling, and metabolic regulation. Functional enrichment and PPI analysis highlighted HMGCR, PCSK9, PPAR-<i>α</i>, and LDLR as key targets. Docking studies revealed that EZN has strong binding affinities with these targets, supporting the structural feasibility of these interactions. In vivo, EZN treatment significantly reduced total cholesterol, triglycerides, LDL, and VLDL levels, while increasing HDL. Compared with simvastatin, EZN exhibited superior lipid-lowering effects with a more favorable liver enzyme profile. Gene expression and ELISA analyses indicated downregulation of HMGCR, PCSK9, and APOB, and upregulation of PPAR-<i>α</i>, LDLR, and SRB, highlighting its multi-target modulation of lipid homeostasis. These findings indicate that EZN exerts broad regulatory effects on lipid metabolism through pleiotropic mechanisms and may represent a promising natural candidate for managing hyperlipidemia.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12849214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084460","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":"Elevated Resting Heart Rate in Hospitalized Patients With Atrial Fibrillation Is Associated With Increased Cardiovascular Risk","authors":"Kangning Han,&nbsp;Xia Li,&nbsp;Biao Fu,&nbsp;Mengmeng Li,&nbsp;Tong Liu,&nbsp;Ying Peng,&nbsp;Jing Liu,&nbsp;Na Yang,&nbsp;Yongchen Hao,&nbsp;Chenxi Jiang,&nbsp;Ribo Tang,&nbsp;Jianzeng Dong,&nbsp;Dong Zhao,&nbsp;Deyong Long,&nbsp;Changsheng Ma","doi":"10.1155/cdr/2106637","DOIUrl":"https://doi.org/10.1155/cdr/2106637","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Effective rate control is important in the management of atrial fibrillation (AF). However, the relationship between resting heart rate (RHR) and adverse outcomes in hospitalized patients remains uncertain.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study was to evaluate the association between RHR and in-hospital outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data from the Improving Care for Cardiovascular Disease in China-AF project from 2014 to 2019 were retrospectively analyzed. The primary outcome was the composite of in-hospital all-cause mortality and in-hospital acute heart failure (AHF). Secondary outcomes included stroke/transient ischemic attack (TIA) and bleeding during hospitalization. Logistic regression analyses were used to assess the association between RHR and outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our study included 12,775 patients hospitalized for AF in 236 hospitals. Logistic regression analyses using different models showed a significant association between RHR exceeding 80 bpm and an increased risk of the primary outcome (adjusted OR: 1.79 [95% CI: 1.44–2.22]). A positive association between RHR and the primary outcome was identified with RHR ≥ 80 bpm. Marginal effect analyses showed that patients with advanced AF types were at higher risk across the range of RHR. Conversely, catheter ablation, but not antiarrhythmic drug use, was associated with a decreased risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>A significant association was identified between RHR and adverse outcomes in patients hospitalized for AF, where RHR exceeding 80 bpm was associated with an increased risk.</p>\u0000 \u0000 <p><b>Trial Registration:</b> ClinicalTrials.gov identifier: NCT02309398</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/2106637","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146058119","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":"The Efficacy and Safety of Four Novel PCSK9 Monoclonal Antibodies in Patients With Hypercholesterolemia: A Systematic Review With Network Meta-Analysis and Trial Sequential Analysis","authors":"Sihua Wang,&nbsp;Chenyu Li,&nbsp;Duncong Fan","doi":"10.1155/cdr/6345873","DOIUrl":"10.1155/cdr/6345873","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>This network meta-analysis (NMA) evaluated four novel proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies for hypercholesterolemia management, comparing their lipid-lowering efficacy and safety.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We systematically identified randomized controlled trials employing the frequentist NMA method to assess reductions in low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), and lipoprotein (a) (Lp[a]), alongside treatment-emergent adverse events (TEAEs) and serious TEAEs. <i>P</i>-scores ranked therapeutic hierarchies, with meta-regression and subgroup analyses exploring heterogeneity. Trial sequential analysis determined the adequacy of cumulative evidence. Confidence in the network meta-analysis approach was used to evaluate the confidence in the findings from NMA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of eight trials with 3,975 Chinese patients were included. Ongericimab 150 mg every 2 weeks (Q2W) ranked first in all efficacy outcomes, demonstrating pronounced effects in LDL-C, ApoB, and Lp(a) reduction versus placebo, with mean differences of −74.21% (95% confidence interval [CI]: −79.69% to −68.73%), −64.36% (95% CI: −68.58% to −60.13%), and −50.93% (95% CI: −56.24% to −45.61%), respectively. All interventions exhibited safety profiles comparable with placebo, with no significant differences in TEAEs or serious TEAEs incidence. The analyses suggested that a portion of the evidence base was robust and reliable.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings positioned ongericimab 150 mg Q2W as a clinically optimal PCSK9 inhibitor with robust lipid-lowering capacity. The results highlight the potential of next-generation PCSK9 monoclonal antibodies, particularly in East Asian populations, while underscoring the need for large-scale multinational trials to validate ethnic-specific responses.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12831481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050121","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":"Nonlinear and Age-Specific Associations Between Atherogenic Index of Plasma and Differential Cardiovascular Risk Profiles in US Adults","authors":"Yuelin Hu,&nbsp;Xuli Chen,&nbsp;Yanchao Liu,&nbsp;Qiuyu Wang,&nbsp;Wenwen Xiao","doi":"10.1155/cdr/6691842","DOIUrl":"10.1155/cdr/6691842","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The association between the atherogenic index of plasma (AIP) and different cardiovascular disease (CVD) outcomes remains insufficiently studied.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data from 16,302 US adults in NHANES 2005–2020 were analyzed. CVD outcomes included congestive heart failure, coronary heart disease, angina, heart attack, and stroke. Multivariable logistic regression models assessed the linear association between AIP and CVD. Restricted cubic splines were used to examine potential nonlinear relationships, whereas threshold effect analysis identified inflection points. Stratified analyses explored interactions between AIP and covariates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with the lowest quartile, the highest AIP quartile was associated with increased odds of overall CVD (OR = 1.73, 95% CI = 1.20–2.52, <i>p</i> for trend = 0.001), coronary heart disease (OR = 2.20, 95% CI = 1.20–4.25, <i>p</i> for trend = 0.013), and heart attack (OR = 2.53, 95% CI = 1.42–4.74, <i>p</i> for trend = 0.008). A U-shaped relationship was observed between AIP and congestive heart failure (<i>p</i> overall = 0.0004, <i>p</i> nonlinear = 0.002), with a sharp odds increase when AIP exceeded 0.22 (OR = 3.40, 95% CI = 1.81–6.38, <i>p</i> &lt; 0.01). Subgroup analysis revealed a significant age interaction: Among adults younger than 55 years, each AIP increment was associated with higher odds of CVD (OR = 2.53, 95% CI = 1.60–3.98, <i>p</i> = 0.001), heart attack (OR = 2.58, 95% CI = 1.21–5.54, <i>p</i> = 0.014), and stroke (OR = 2.98, 95% CI = 1.44–6.17, <i>p</i> = 0.003).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Elevated AIP is an independent predictor of CVD, coronary heart disease, and heart attack, particularly in younger adults (&lt; 55 years). A U-shaped relationship was identified between AIP and congestive heart failure. These findings highlight AIP as a valuable biomarker for CVD risk assessment and emphasize the importance of age-specific intervention strategies targeting different CVD outcomes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050103","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":"From the Liver to Heart in Nonalcoholic Fatty Liver Disease: Single-Cell and Serum Evidence for Cytokeratin 18 in Predicting Cardiovascular Risk","authors":"Hongjing Xu,&nbsp;Xiang Ma,&nbsp;Fengjuan Chen,&nbsp;Bin Zhou","doi":"10.1155/cdr/3055531","DOIUrl":"10.1155/cdr/3055531","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This study is aimed at measuring the expression of serum cytokeratin 18 (CK18) in patients with nonalcoholic fatty liver disease (NAFLD) and at evaluating its ability to discriminate NAFLD patients with and without coronary heart disease (CHD), thereby elucidating its potential role in reflecting the link between NAFLD and increased cardiovascular involvement.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 127 patients diagnosed with NAFLD and treated between September 2022 and July 2024 were enrolled in this cross-sectional study. Based on the presence or absence of CHD, they were divided into two subgroups: a CHD-present group (<i>n</i> = 79) and a CHD-absent group (<i>n</i> = 48). In addition, a control group consisting of 100 age-matched and sex-matched healthy individuals undergoing routine physical examinations during the same period was included for comparison.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with the control group, patients with NAFLD showed significantly higher levels of alanine aminotransferase (ALT), serum CK18-M65 and CK18-M30 levels, body mass index (BMI), homeostasis model assessment of insulin resistance index (HOMA-IR), triglyceride (TG), total cholesterol (TC), aspartate aminotransferase (AST), and waist-to-hip ratio (<i>p</i> &lt; 0.05). Multivariate logistic regression analysis identified serum CK18-M65, CK18-M30, TC, ALT, AST, and HOMA-IR as independent factors in NAFLD patients (<i>p</i> &lt; 0.05). The combination of CK18-M65 and CK18-M30 yielded an area under the curve of 0.843, with a sensitivity of 87.34% and a specificity of 75.00%. Functional enrichment analysis revealed that CK18-related genes were involved in inflammatory signaling and cardiovascular regulatory pathways, supporting a mechanistic role for CK18 in the liver–heart axis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Serum CK18 may serve as a useful biomarker for identifying NAFLD patients with concurrent CHD, offering diagnostic value in clinical assessment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12808931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997427","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 ALDH2 Gene Polymorphism and Coronary Artery Disease in Patients With Atrial Fibrillation","authors":"Bo Zheng,&nbsp;Meiling Li,&nbsp;Peng Wang,&nbsp;Jialong Lin,&nbsp;Haifeng Pei,&nbsp;Hao Liu,&nbsp;Xianglin Ye","doi":"10.1155/cdr/8733628","DOIUrl":"10.1155/cdr/8733628","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>The objectives of this study is to investigate the correlation between genotype polymorphism of aldehyde dehydrogenase 2 (ALDH2) and coronary artery disease (CAD) in atrial fibrillation patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>From November 2020 to December 2021, 80 patients with atrial fibrillation at a medical center in Chengdu were divided into two groups: CAD group (<i>n</i> = 25) and non-CAD group (<i>n</i> = 55). The genotype composition ratio of ALDH2 (mutant-type/wild-type), blood biochemical indexes, the proportion of the history of lipid-lowering drugs and time of taking lipid-lowering drug were compared between the two groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The CAD group showed significantly lower levels of total cholesterol and low-density lipoprotein cholesterol (LDL-C) compared with the non-CAD group (<i>p</i> &lt; 0.05), and the proportion and time of taking lipid-lowering drugs in CAD group were significantly increased (<i>p</i> &lt; 0.05). The frequency of the ALDH2 genotype (mutant-type/wild-type) in the CAD group was notably elevated compared with that in the non-CAD group (<i>p</i> &lt; 0.05). In patients with atrial fibrillation, the risk of CAD in patients with ALDH2 mutant genotype (GA + AA) was 5.849 times that of ALDH2 wild-type genotype (GG) (95<i>%</i>CI = 1.437–23.795, <i>p</i> &lt; 0.05). The area under ROC curve of ALDH2 mutant genotype (GA + AA) was 0.624 (SE = 0.069, 95<i>%</i>CI : 0.488–0.759). In patients with ALDH2 wild-type (GG), the levels of total cholesterol and LDL-C in CAD group were significantly lower than those in non-CAD group (<i>p</i> &lt; 0.05). However, in patients with ALDH2 mutation genotype (GA + AA), the proportion of history of lipid-lowering drugs in CAD group was significantly higher than that in non-CAD group (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The polymorphism of ALDH2 gene is a high risk factor for CAD in patients with atrial fibrillation. The ALDH2 mutation genotype (GA + AA) may reduce the lipid-lowering efficacy of statins.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12808927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997389","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":"Aldehyde Dehydrogenase-2 Alleviates Septic Myocardial Injury by Inhibiting Caspase-11-Mediated Noncanonical Pyroptosis","authors":"Huan Liang,&nbsp;Yuying He,&nbsp;Yiren Wang,&nbsp;Rui Zhang,&nbsp;Mengjie Yu,&nbsp;Hongwei Ye,&nbsp;JiaHui Wang,&nbsp;Qin Gao","doi":"10.1155/cdr/5289405","DOIUrl":"10.1155/cdr/5289405","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>The purpose of this study is to investigate the role of aldehyde dehydrogenase-2 (ALDH2) in septic myocardial injury, focusing on noncanonical pyroptosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In vivo, C57BL/6J mice were divided into five groups: Sham, cecal ligation and puncture (CLP), CLP + Alda-1 (ALDH2 agonist), Sham + dimethyl sulfoxide (DMSO, solvent control), and CLP + DMSO. Cardiac function and histological/ultrastructural changes were assessed via echocardiography, hematoxylin–eosin (HE) staining, and transmission electron microscopy (TEM). Tumor necrosis factor-<i>α</i> (TNF-<i>α</i>) and noncanonical pyroptosis-related proteins (caspase-11, gasdermin-D [GSDMD], high mobility group box 1 [HMGB1], and receptor for advanced glycation end products [RAGE]) were measured by enzyme-linked immunosorbent assay (ELISA) and western blotting. Coimmunoprecipitation (CO-IP) explored molecular mechanisms. In vitro, H9C2 cells were divided into six groups: Control, lipopolysaccharide (LPS)-treated, ALDH2-green fluorescent protein (GFP), LPS + ALDH2-GFP, GFP, and GFP + LPS. Cell viability, lactate dehydrogenase (LDH) release, creatine kinase isoenzymes (CK-MB), and target protein levels were detected via spectrophotometry, western blotting, and immunofluorescence (IF).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In vivo, Alda-1 significantly attenuated CLP-induced cardiac dysfunction and reduced myocardial histological damage and ultrastructural impairment. In vitro, ALDH2 overexpression lowered LPS-induced H9C2 cell viability, CK-MB, and LDH release. Upregulating ALDH2 significantly reduced caspase-11, HMGB1, and RAGE expression. CO-IP showed ALDH2 interacted with HMGB1, RAGE, and GSDMD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>ALDH2 protects the myocardium from septic injury by inhibiting caspase-11-mediated noncanonical pyroptosis, possibly via direct interactions with GSDMD, HMGB1, and RAGE.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12800742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988433","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}