Journal of Cardiovascular Pharmacology最新文献

{"title":"Cardioprotective effects of soluble guanylate cyclase and its α1 subunit on myocardial ischemia/reperfusion injury via the PGC-1α/UCP2 pathway.","authors":"Jiao Li, Xinhang Li, Yafang Chen, Linlin Fang, Qi Li, Hao Wu, Yue Liu, Xin Qi, Liping Wei","doi":"10.1097/FJC.0000000000001765","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001765","url":null,"abstract":"<p><p>This study investigates the cardioprotective potential of soluble guanylate cyclase (sGC) and its α1 subunit in myocardial ischemia/reperfusion (I/R) injury, along with the underlying mechanisms. We used a model involving Sprague Dawley rats undergoing left coronary artery I/R, complemented by H9c2 cell cultures in an anaerobic environment to simulate I/R conditions in vitro. Both loss- and gain-of-function approaches were applied to assess the role of sGC and its α1 subunit in myocardial I/R injury. Immunofluorescence microscopy, Western blotting, and RT-PCR were employed to examine how sGC and its α1 subunit influence oxidative stress and apoptosis. Our results showed that sGC and its α1 subunit were associated with reduced I/R injury severity in both in vitro and in vivo settings. Overexpression of sGC decreased cardiomyocyte apoptosis and maintained mitochondrial function during I/R, while sGC silencing heightened oxidative stress and apoptosis. Additionally, pharmacological modulation of sGC impacted signaling in the PGC-1α/UCP2 pathway. These findings demonstrate the crucial role of sGC and its α1 subunit in protecting against cardiac injury during I/R, suggesting that sGC-targeted therapies could offer promising strategies for managing myocardial damage associated with I/R injury.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145280188","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":"Commentary On the Effects of Anakinra on Cardiorespiratory Fitness in Heart Failure Stratified by Age in Phase II Clinical Trials.","authors":"Davide Nilo, Francesca Gualdiero, Vincenzo Russo, Katarzyna Zielińska, Ferdinando Carlo Sasso, Alfredo Caturano","doi":"10.1097/FJC.0000000000001767","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001767","url":null,"abstract":"","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274720","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":"NOX-derived ROS generation drives endothelial-to-mesenchymal transition in human pulmonary endothelial cells exposed to sera from patients with idiopathic pulmonary fibrosis.","authors":"Thị Hằng Giang Phan, Anna Maria Posadino, Roberta Giordo, Alessandro Giuseppe Fois, Pietro Pirina, Angelo Zinellu, Ali Hussein Eid, Gianfranco Pintus","doi":"10.1097/FJC.0000000000001764","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001764","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive lung disease marked by extracellular matrix deposition, oxidative stress, and profound microvascular remodeling. Endothelial dysfunction, particularly via endothelial-to-mesenchymal transition (EndMT), has been implicated in fibrotic progression but remains insufficiently characterized. In this study, human pulmonary microvascular endothelial cells (HPMECs) were exposed to 5% serum from patients with IPF or healthy donors to model disease-associated vascular alterations. IPF serum stimulated a robust increase in reactive oxygen species (ROS) production and proliferation, concomitant with downregulation of endothelial markers (von Willebrand factor, CD31) and upregulation of mesenchymal markers (α-smooth muscle actin, collagen I), consistent with EndMT induction. Notably, pharmacological inhibition of NADPH oxidase (NOX) with diphenyleneiodonium markedly attenuated ROS generation, phenotypic switching, and junctional disruption observed under IPF serum exposure. Similarly, inhibition of protein kinase C (PKC) by chelerythrine suppressed ROS production and proliferative responses, implicating PKC-dependent pathways in ROS-mediated endothelial injury. Immunofluorescence analyses confirmed structural reorganization, revealing loss of endothelial junctional integrity and accumulation of mesenchymal proteins, both reversed by NOX inhibition. Together, these findings establish IPF serum-derived factors as potent drivers of endothelial oxidative stress and EndMT via NOX- and PKC-dependent mechanisms. Targeting these redox-sensitive pathways may represent a promising therapeutic strategy to mitigate vascular dysfunction, tissue remodeling, and disease progression in IPF.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244726","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":"Nrf2/ARE pathway agonist omaveloxolone attenuates adverse cardiac remodeling in pressure-induced cardiac dysfunction.","authors":"Alexander E Berezin","doi":"10.1097/FJC.0000000000001763","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001763","url":null,"abstract":"","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244736","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":"Genetic and Epigenetic Biomarkers in Hypertension Impact on the Effectiveness of Individualized Therapy: A Systematic Review.","authors":"Anderson Matheus Pereira da Silva, Elaine da Silva Torres, Maria da Vitória Santos do Nascimento, Julia Oliveira Franco, Dillan Cunha Amaral, Anderson Silva Corin, Lívia Barbosa Cavalcanti, Maria Bernadete de Sousa Maia, Eryvelton de Souza Franco","doi":"10.1097/FJC.0000000000001743","DOIUrl":"10.1097/FJC.0000000000001743","url":null,"abstract":"<p><strong>Abstract: </strong>Arterial hypertension affects >1.28 billion adults globally, remaining a leading cause of cardiovascular morbidity and mortality. Despite effective therapies, suboptimal blood pressure control persists, highlighting the need for precision approaches. Epigenetic biomarkers, particularly DNA methylation (DNAm), have emerged as potential tools to enhance risk stratification and personalize antihypertensive therapy, yet their clinical relevance remains uncertain. To systematically synthesize evidence on genetic and epigenetic biomarkers associated with hypertension, focusing on DNAm signatures, regulatory pathways, and translational potential, we conducted a systematic review and meta-analysis following Preferred Reporting Items for Systematic Review and Meta-Analysis guidelines, registered in PROSPERO (Chronic Renal Disease (CRD) 420251059256). PubMed, MEDLINE, Embase, and ScienceDirect were searched up to March 2025. Eligible studies investigated genetic or epigenetic markers, such as DNAm, single nucleotide polymorphisms, or chromatin modifications in adult hypertension populations. Data on study design, populations, biomarkers, analytical methods, and outcomes were extracted. Risk of bias was assessed using RoB 2 and Risk of Bias in Nonrandomized Studies of Interventions tool. Twelve studies were included, encompassing cross-sectional and longitudinal designs. DNAm signatures at loci including AGTR1, PHGDH, SLC7A11, Angiotensin-Converting Enzyme (ACE), and WNT3A were recurrently associated with blood pressure regulation. Transancestry genome-wide analyses identified methylation-enriched loci such as KCNK3, PDE3A, and PRDM6. However, no study demonstrated predictive value for clinical end points or robust replication across diverse populations. Methodological heterogeneity limited longitudinal data and underrepresentation of low- and middle-income countries were key limitations. Although epigenetic markers show promise for hypertension research, current evidence remains exploratory. Rigorous, longitudinal studies integrating clinical end points are essential for advancing toward clinical translation.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"321-329"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144731128","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":"Dihydrotestosterone Pretreatment Diminishes the Severity of Drug-Induced Torsades de Pointes.","authors":"James E Tisdale, Heather A Jaynes, Brian R Overholser, Kevin M Sowinski, Richard J Kovacs","doi":"10.1097/FJC.0000000000001716","DOIUrl":"10.1097/FJC.0000000000001716","url":null,"abstract":"<p><strong>Abstract: </strong>Testosterone and dihydrotestosterone (DHT) attenuate drug-induced lengthening of ventricular repolarization, but it is unknown whether they influence drug-induced torsades de pointes (TdP). We tested the hypothesis that DHT reduces the incidence and severity of drug-induced TdP. Male New Zealand white rabbits underwent orchiectomy and were implanted with 2 subcutaneous sustained-release pellets containing DHT 50 mg (100 mg, n = 23) or placebo (n = 20). After 7 days, hearts were excised, mounted, and perfused with modified Krebs-Henseleit solution. The atrioventricular node was destroyed manually. Dofetilide 100 nM was perfused for 30 minutes. Median (Q 1 , Q 3 ) serum DHT concentrations were higher in DHT-treated rabbits [314.0 (232.5, 388.6) vs. 32.5 (28.5, 36.2) ng/dL, P < 0.0001]. The incidence of TdP in the DHT and placebo groups was 6/23 (26%) versus 8/20 (40%), respectively ( P = 0.33). In hearts that developed TdP, the median (Q 1 , Q3) number of episodes was lower in the DHT group [2 (2, 3.5) vs. 18.5 (12.5, 20.5), P = 0.01]. The median time to first TdP episode was longer [18.5 (17.3, 21.3) vs. 10.5 (12.5, 20.5) minutes, P = 0.01], and the TdP burden (median total number of TdP beats per heart) was lower in the DHT group [11.5 (9.5-46.5) vs. 271 (99.3-440.3) beats, P = 0.007]. Pre-dofetilide Fridericia-corrected QT intervals were shorter in the DHT group [377 (366, 390) vs. 385 (378, 401) ms, P = 0.02]. Maximum Fridericia-corrected QT interval during dofetilide perfusion was shorter in the DHT group [399 (390, 410) vs. 414 (399, 442) ms, P = 0.007]. In conclusion, DHT diminishes the severity of dofetilide-induced TdP.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"343-349"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12353403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019598","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":"Perspectives on Artificial Intelligence in Medical Publishing: A Survey of Medical Journal Editors.","authors":"Giuseppe Biondi-Zoccai, Attilio Lauretti, Stefan Agewall, Emmanuel Andres, Riccardo A Audisio, Deepak L Bhatt, Giuseppe Citerio, Jonathan A Drezner, Alexander Eggermont, Cetin Erol, Karen D Ersche, Giorgio Ferriero, Gerd Heusch, Ciro Indolfi, Paul A Insel, Carl J Lavie, Carlo La Vecchia, Nicola Maffulli, Fabrizio Montecucco, David J Moliterno, Stanley Nattel, Peter O'Kane, Elena Oliaro, Antonio Pelliccia, Michael Picard, Paolo Pozzilli, Fabiana Quaglia, Renata L Riha, Rupa Sarkar, Pietro Scicchitano, Jean-Louis Teboul, Hendrik Tevaearai Stahel, Loren E Wold, George W Booz","doi":"10.1097/FJC.0000000000001738","DOIUrl":"10.1097/FJC.0000000000001738","url":null,"abstract":"<p><strong>Abstract: </strong>Artificial intelligence (AI) has been increasingly integrated into medical publishing, hopefully improving efficiency and accuracy, but serious concerns persist regarding ethical implications, authorship attribution, and content reliability. We aimed at understanding the perspectives of editors of medical journals on AI. A structured online questionnaire was developed and distributed to editors-in-chief of medical journals worldwide. The survey comprised 27 concise questions exploring demographics, journal practices, and perspectives on AI in editorial workflows. Quantitative data were analyzed using descriptive statistics to summarize usage patterns, perceived benefits, risks, and future expectations. A total of 59 editors-in-chief completed the survey (response rate: 19%), with replies suggesting substantial variability in beliefs and attitudes toward AI for publication in medical journals. Artificial intelligence tools were already in use by 49% of journals, mainly for plagiarism detection (76%) and data verification (35%). Only 9% of responders reported that journals used AI for both scientific and linguistic review. Time savings (79%) and cost reduction (43%) were the most commonly cited benefits, and concerns included potential bias (71%) and lack of accountability (60%). Overall, 81% of responders anticipated a major role for AI in publishing within 10 years. Exploratory analyses suggested several potential associations between replies and respondent or journal features, requiring further validation in future surveys. In conclusion, this survey on attitudes toward AI in publication in medical journals suggests that editors-in-chief are cautiously adopting AI in their editorial workflow, supporting its operational use while explicitly calling for clear guidance to address ethical and regulatory concerns.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"374-383"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12499947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690395","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":"Intrapericardial Bleomycin for Malignant Pericardial Effusion: Revisiting a Targeted Pharmacologic Approach.","authors":"Danny L Rayes, Hira Latif, Syed Waqas Haider","doi":"10.1097/FJC.0000000000001746","DOIUrl":"10.1097/FJC.0000000000001746","url":null,"abstract":"","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"337-339"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742198","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":"Fibroblast Activation Protein Promotes Pulmonary Artery Hypertension via Activation of the PTEN/PI3K/Akt Pathway.","authors":"Minghui Zhu, Fei Xu, Le Zhu, Qianqian Chen, Xiaomin Jiang, Chang Pan, Wande Yu, Hang Zhang","doi":"10.1097/FJC.0000000000001735","DOIUrl":"10.1097/FJC.0000000000001735","url":null,"abstract":"<p><strong>Abstract: </strong>Pulmonary arterial hypertension (PAH) is a severe disease characterized by significant pulmonary vascular remodeling and right ventricular dysfunction. Activated fibroblasts can induce collagen deposition around blood vessels, thereby promoting vascular hardening and PAH development. Fibroblast activation protein (FAP) is a proline-specific serine protease expressed in active fibroblasts that is closely associated with tissue remodeling, inflammation, fibrosis, tumor growth, and cellular proliferation. However, whether FAP is linked to PAH has not yet been addressed. This study aimed to investigate the potential role of FAP in PAH pathogenesis. In animal models of PAH, we found that FAP expression levels were higher both in vivo and in vitro than in the control group. And FAP inhibitors alleviated pulmonary vascular remodeling and right ventricular function in vivo PAH model. To explain the elevated expression of FAP in PAH, we screened the transcription factor Egr1 of FAP through the databases GTRD and Human TFDB, and demonstrated that the transcriptional activity of early growth response 1 (Egr1) binds to the FAP promoter region and regulates FAP by chromatin immunoprecipitation assay and the dual-luciferase reporter gene assay. Subsequently, we demonstrated that FAP promotes the activation of pulmonary arterial adventitial fibroblasts by enhancing their proliferation, migration, and transformation into muscle fibroblasts. Furthermore, FAP mechanistically affects the PTEN/PI3K/Akt signaling pathway, which is a classic signaling pathway that regulates fibroblast proliferation, migration, and invasion. In summary, FAP plays a crucial role in activating pulmonary arterial adventitial fibroblasts and may be a potential therapeutic target for patients with PAH.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"391-407"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659335","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":"Bleomycin for Malignant Pericardial Effusion: A Systematic Review of Efficacy and Adverse Events.","authors":"Paulus Parholong Siahaan, Roy Bagus Kurniawan, Pandit Bagus Tri Saputra, Jannatin Nisa Arnindita, Cornelia Ghea Savitri, Luqman Hakim Andira, Estya Nadya Meitavany, Johanes Nugroho Eko Putranto, Firas Farisi Alkaff","doi":"10.1097/FJC.0000000000001713","DOIUrl":"10.1097/FJC.0000000000001713","url":null,"abstract":"<p><strong>Abstract: </strong>Malignant pericardial effusion (MPE) is a progressive fluid accumulation in the pericardial space that can lead to pericardial tamponade. Despite the high recurrence rate associated with pericardiocentesis, it remains the mainstay therapy. Bleomycin has emerged as an intrapericardial sclerosing therapy that may reduce recurrence and improve patients' quality of life. This systematic review aimed to assess the efficacy and safety profile of bleomycin instillation in patients with MPE. An exhaustive search was conducted in PubMed, Web of Science, Scopus, ProQuest, EBSCO, and ClinicalTrials.gov databases. Eligible studies included MPE patients as participants who were treated with intrapericardial bleomycin, reporting the patients' outcomes and using English in the full text. Individual studies were assessed for quality using the Newcastle-Ottawa Scales for cohort studies and the Jadad Scale for trial studies. Eight studies were included in this systematic review involving 242 MPE patients treated with bleomycin. Bleomycin demonstrated lower recurrence rates than other sclerosing agents, with only ≤5% of patients requiring repeated drainage because of recurrence. Bleomycin treatment resulted in 3.5 days less hospitalization compared with doxycycline. Bleomycin is also safe to use, with reported less severe pain compared with other treatment agents for MPE, such as doxycycline and pericardiocentesis. Bleomycin may benefit patients by reducing recurrence rates and improving patients' quality of life. Moreover, it is safe and has low rates of adverse events after the instillation.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"330-336"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101154","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}