Cardiology Plus最新文献

{"title":"Histological validation of artificial intelligence-driven automatic plaque characterization in coronary OCT: a head-to-head comparison with clinicians.","authors":"Miao Chu, Francesca Razzi, Giovanni Luigi De Maria, Stefano Benenati, Jason Chai, Wei Yu, Ruobing Dai, Volkert van Steijn, Adrian Banning, Juan Luis Gutiérrez-Chico, Shengxian Tu, Heleen van Beusekom","doi":"10.1097/CP9.0000000000000158","DOIUrl":"10.1097/CP9.0000000000000158","url":null,"abstract":"<p><strong>Background and purpose: </strong>Artificial intelligence (AI) is increasingly being applied to automate image interpretation, including in coronary optical coherence tomography (OCT), the gold standard for in vivo assessment of atherosclerotic plaques. Most AI models are trained using expert annotations; however, human interpretation is inherently subjective and may limit model performance. Therefore, validation against the true reference standard-histology-remains essential. The study aims to evaluate and compare the performance of an AI-powered plaque characterization model with that of clinicians, using co-registered histology as the reference standard.</p><p><strong>Methods: </strong>Matched OCT pullbacks and serial histological sections from 25 plaques in 11 swine atherosclerotic arteries were analyzed. Precise OCT-histology co-registration was achieved using a hierarchical coarse-to-fine approach, with stent edges and anatomical landmarks as references. Plaque components (fibrous, lipidic, and calcific) were manually labeled on histology and automatically segmented on OCT by the AI model. Meanwhile, three blinded readers with different levels of OCT expertise independently annotated the corresponding frames. The relative percentages of plaque components derived from OCT were compared with histology.</p><p><strong>Results: </strong>Across all histological sections, the median percentages of fibrous, lipidic, and calcific components were 65.0% (interquartile range [IQR]: 53.9%-92.5%), 34.3% (IQR: 6.5%-44.7%), and 0.2% (IQR: 0%-1.9%), respectively. The AI model demonstrated excellent correlation with histology, with Spearman's <i>ρ</i> = 0.907 (P < 0.001) for fibrous and <i>ρ</i> = 0.900 (P < 0.001) for lipidic components. The mean absolute discrepancy relative to histology was comparable between the AI model and the senior reader and smaller than that of the intermediate and junior readers. Agreement with histology improved with reader's experience (fibrous: intraclass correlation coefficients [ICC] = 0.666, 0.720, and 0.821; lipidic: ICC = 0.593, 0.684, and 0.803), yet remained lower than that of the AI model (fibrous: ICC = 0.938; lipidic: ICC = 0.939).</p><p><strong>Conclusions: </strong>Despite being trained on human-annotated data, the AI model demonstrated superior agreement with histology compared with clinicians. AI-driven plaque characterization may reduce interpretative subjectivity and enhance the clinical utility of coronary OCT in the management of coronary artery disease.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"11 2","pages":"102-110"},"PeriodicalIF":2.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13299032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148347161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond autophagic flux: selective autophagy adaptors and cargo prioritization in cardiac disease.","authors":"Jenaro A Espitia-Corredor, Francisco Olivares-Silva, Constanza Alanis-Cubillos, Yingfeng Deng, Zhao V Wang","doi":"10.1097/CP9.0000000000000161","DOIUrl":"10.1097/CP9.0000000000000161","url":null,"abstract":"<p><p>Cardiovascular disease is the leading cause of death worldwide. Disrupted protein homeostasis contributes significantly to cardiomyocyte dysfunction and loss. While autophagy is recognized as a critical cardioprotective mechanism, most therapeutic strategies have targeted overall autophagic flux, assuming that increasing degradative capacity is inherently beneficial. This approach overlooks a fundamental question: when multiple substrates compete for limited autophagic capacity, what determines which cargo is prioritized? This review focuses on the selective autophagy adaptors (sequestosome 1 [p62/SQSTM1], neighbor of BRCA1 gene 1 [NBR1], Tax1-binding protein 1 [TAX1BP1], optineurin [OPTN], nuclear dot protein 52 kDa [NDP52], and Fab1, YOTB, Vac1, EEA1 domain, and coiled-coil domain containing 1 [FYCO1]) as the molecular machinery governing cargo selectivity. We synthesize evidence demonstrating that adult cardiomyocytes face a unique \"triage problem\": as post-mitotic cells with a massive proteome and high metabolic demands, they must continuously prioritize which damaged mitochondria, protein aggregates, or sarcomeric components to eliminate. We integrate findings from cardiac studies with mechanistic insights from other cell types to map adaptor function in the heart. We propose that targeting selective autophagy adaptors may offer therapeutic precision beyond global flux modulation, directing autophagic machinery toward the cargo most relevant to individual pathological contexts. Currently, FYCO1 overexpression remains the only adaptor-level intervention validated to rescue cardiac function in vivo, highlighting both proof-of-concept and substantial opportunity for further investigation. Understanding not just how much the heart degrades, but also what it chooses to degrade may open new avenues for treating heart failure and cardiomyopathies.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"11 2","pages":"134-150"},"PeriodicalIF":2.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13299037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148347115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing cardio-oncology: precision-guided cardiovascular care for oncology patients.","authors":"Jennifer E Liu","doi":"10.1097/CP9.0000000000000142","DOIUrl":"10.1097/CP9.0000000000000142","url":null,"abstract":"<p><p>Cardio-oncology, an emerging subspecialty at the intersection of cardiology and oncology, addresses the growing cardiovascular burden among cancer patients and survivors. Advances in cancer therapies, including anthracyclines, immune checkpoint inhibitors (ICIs), chimeric antigen receptor (CAR) T-cell therapy, and targeted tyrosine kinase inhibitors (TKIs), have improved survival but also introduced diverse cardiovascular complications such as heart failure, arrhythmias, hypertension, and ischemia. These complications are influenced by traditional cardiovascular risk factors, aging, and comorbidities, underscoring the need for precision-guided risk assessment and management. Recent innovations in cardio-oncology focus on personalized risk stratification using clinical risk models, genetic profiling, and emerging biomarkers such as high-sensitivity troponin, natriuretic peptides, and microRNAs. Advanced imaging modalities, including echocardiography, global longitudinal strain analysis, and cardiac magnetic resonance, are central to early detection of subclinical injury, with artificial intelligence (AI) increasingly enabling real-time, individualized surveillance. The integration of novel biological insights, such as clonal hematopoiesis of indeterminate potential, further refines risk prediction and mechanistic understanding. Effective cardio-oncology care requires proactive, multidisciplinary strategies that span the continuum from treatment initiation to survivorship, emphasizing longitudinal monitoring, cardioprotective interventions, and patient-centered care. Despite progress, challenges remain in standardizing predictive models, validating biomarkers, and ensuring equitable access to specialized services. Looking forward, the convergence of AI-driven imaging, multi-omic data, and precision therapeutics promises to transform cardio-oncology from reactive management to proactive, personalized care, optimizing both cancer outcomes and long-term cardiovascular health.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 4","pages":"241-245"},"PeriodicalIF":0.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12753144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145879459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between immune checkpoint inhibitors and adverse cardiovascular events in patients with coronary artery disease and malignant tumors: a retrospective cohort study.","authors":"Ran Xu, Yan Wang, Qingqing Cai, Hao Lu, Leilei Cheng","doi":"10.1097/CP9.0000000000000135","DOIUrl":"10.1097/CP9.0000000000000135","url":null,"abstract":"<p><strong>Background and purpose: </strong>With the widespread application of immune checkpoint inhibitors (ICIs) in cancer treatment, the associated risk of developing atherosclerotic cardiovascular injury is increasing. However, the risk of cardiovascular disease after ICI treatment in patients with both coronary artery disease and malignancy remains unclear. This study aimed to investigate whether ICI treatment is associated with an increased risk of major adverse cardiovascular events (MACE) in these high-risk patients.</p><p><strong>Methods: </strong>This single-center, retrospective cohort study included 93 patients diagnosed with coronary heart disease and malignant tumors who received ICIs or non-ICIs therapy. The primary outcome was MACE, defined as a composite of cardiogenic death, heart failure, non-fatal acute coronary syndrome, and non-fatal ischemic stroke. The association between baseline clinical parameters, including ICI exposure, and the incidence of MACE was evaluated.</p><p><strong>Results: </strong>During a median follow-up of 14 months, MACE occurred in 32.50% of ICIs-treated patients, with a median time to event of 4 months (2.0-8.5 months), compared to 11.32% and 15.5 months (7.8-27.0 months) in non-ICIs patients. Additionally, all-cause mortality occurred in 12.50% of the ICIs-treated group and 13.21% of the non-ICIs group. Traditional cardiovascular risk factors were not associated with MACE in patients with or without ICI treatment. Multivariable regression analyses revealed an increased risk of developing MACE following ICIs therapy (hazard ration [HR]: 2.86, 95% confidence interval [95% CI]: 1.01-8.11; P = 0.048).</p><p><strong>Conclusions: </strong>Our findings show that ICIs therapy may be independently associated with an increased risk of MACE in patients with coronary heart disease and malignancy. Further larger-scale studies are needed to validate the potential cardiotoxic risk associated with ICIs.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 4","pages":"253-260"},"PeriodicalIF":0.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12753147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145879121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coronary physiology in the catheterization laboratory: current practices, historical insights, and future directions.","authors":"Simone Fezzi, Carlotta Rossignoli, Ludovica Guerrieri, Daixin Ding, Jiayue Huang, Gabriele Pesarini, Domenico Tavella, Roberto Scarsini, Flavio Ribichini, William Wijns, Shengxian Tu","doi":"10.1097/CP9.0000000000000131","DOIUrl":"10.1097/CP9.0000000000000131","url":null,"abstract":"<p><p>Coronary flow improvement and myocardial ischemia relief are the primary goals of coronary revascularization. The pioneering work of Andreas Gruntzig, who demonstrated the reduction of trans-stenotic pressure gradients following percutaneous coronary intervention (PCI), marked a major milestone in the field. Since then, a variety of invasive and non-invasive techniques for assessing coronary physiology have been developed. These methods play a pivotal role in evaluating the hemodynamic significance of coronary lesions, guiding PCI planning, optimizing post-PCI outcomes, and assessing coronary microcirculation and disease patterns. This review explores the available tools for coronary physiology assessment in the catheterization laboratory and their applications in the decision-making process for coronary revascularization. In addition, it highlights recent technological advances, such as invasive and coronary image-based computational methods. These innovations enable individualized PCI treatment, aiming for complete ischemia relief through optimized morpho-functional procedural outcomes.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 3","pages":"217-234"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12487665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell transcriptomics reveals Cdh2–Vegfa-mediated myocyte communication as a mechanism of empagliflozin in heart failure with preserved ejection fraction","authors":"Mingying Deng, Xiayun Ni, Shuo Chen, Yang Zhang, Xiaojun Feng, Zhihua Wang","doi":"10.1097/cp9.0000000000000132","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000132","url":null,"abstract":"Background and purpose: Heart failure with preserved ejection fraction (HFpEF) poses a significant clinical challenge due to limited therapeutic options. Recent clinical trials have highlighted the potential benefits of empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, in patients with HFpEF; however, the molecular mechanisms mediating these effects remain elusive. This study aimed to unravel the molecular mechanisms by which empagliflozin exerts its therapeutic effects in HFpEF. Methods: Using a classical mouse model of HFpEF, we applied single-nucleus ribonucleic acid-sequencing (snRNA-seq) to comprehensively assess the impact of empagliflozin administration and subsequent withdrawal on myocardial tissue single-cell populations. Differentially expressed genes across various biological pathways were identified, and bioinformatics analyses were performed to uncover cellular interactions and signaling cascades modulated by empagliflozin. Results: Empagliflozin treatment significantly altered the expression of genes related to cardiac muscle contraction, neurodegeneration, fluid shear stress and atherosclerosis, and oxidative phosphorylation. Correlation analysis suggested that empagliflozin promoted communication between myocytes (MCs) and both Schwann cells (SCs) and endothelial cells (ECs) via cadherin-2 (Cdh2) and vascular endothelial growth factor A (Vegfa), contributing to improved cardiac function in HFpEF. Western blot confirmed that empagliflozin reversed the downregulation of Cdh2, Vegfa, and vascular endothelial growth factor receptor 2 (Vegfr2). Conclusions: SCs are implicated in HFpEF pathophysiology, and Cdh2 and Vegfa are identified as potential targets through which empagliflozin enhances MC, SC and MC, EC communication to improve cardiac function. These findings provide new insights into the pathogenesis of HFpEF and the mechanisms underlying empagliflozin therapy.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 3","pages":"159-171"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA-ssisting immunity to heal the heart: a new frontier in therapeutics.","authors":"Joel Gregory Rurik, Christian Le Phu, Julian Mustroph, Marcus Buggert","doi":"10.1097/CP9.0000000000000116","DOIUrl":"10.1097/CP9.0000000000000116","url":null,"abstract":"<p><p>Cardiovascular diseases remain the leading cause of death worldwide. Despite significant progress and the development of numerous effective drugs, substantial morbidity and mortality persist. This review highlights one potentially fruitful avenue for discovering novel therapeutics: leveraging ribonucleic acid (RNA) to tip the immunological balance toward tissue repair. Decades of research have primed the three disciplines of cardiology, immunology, and RNA drug development, to bring potent intersectional therapies to the clinic. We discuss both coding and non-coding RNA interventions across multiple cell types, such as monocytes, macrophages, and T cells, throughout different cardiovascular diseases. Altogether, advanced RNA-based medicines targeting the immune system are primed to transform how cardiovascular diseases are treated.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 2","pages":"129-144"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rats subject to extracorporeal membrane oxygenation have improved cardiac function following anticoagulation and reversal with factor IXa aptamer-antidote oligonucleotide pair.","authors":"Shahid M Nimjee, Fellery de Lange, George A Pitoc, Bruce A Sullenger","doi":"10.1097/CP9.0000000000000122","DOIUrl":"10.1097/CP9.0000000000000122","url":null,"abstract":"<p><strong>Background and purpose: </strong>Unfractionated heparin (UFH) is the most commonly utilized rapid-onset anticoagulant, valued for its potency and reversibility with protamine. However, UFH and protamine are associated with significant side effects, including increased morbidity and mortality, and concerns about sustainability due to the environmental impact of large-scale pig farming for heparin production. This study evaluates an alternative anticoagulant strategy using a factor IXa (FIXa) aptamer paired with a matched oligonucleotide antidote, comparing its efficacy and safety to heparin-protamine in a rat extracorporeal membrane oxygenation (ECMO) model.</p><p><strong>Methods: </strong>Twenty-four Sprague-Dawley rats were randomized into two groups: one receiving heparin (600 IU/kg) and protamine (1 mg/100 IU heparin), and the other receiving a cholesterol-modified FIXa aptamer (10 mg/kg) and its antidote (50 mg/kg). Coagulation parameters, platelet counts, inflammatory markers, cardiac function, and histopathology were assessed during and after 60 minutes of ECMO.</p><p><strong>Results: </strong>The FIXa aptamer effectively maintained circuit patency without clot formation, comparable to heparin. The antidote rapidly reversed the aptamer's anticoagulant activity, similar to protamine's reversal of heparin. Notably, the aptamer-antidote group demonstrated superior outcomes, including improved mean arterial pressure (58 ± 6 mmHg vs. 54 ± 3 mmHg at 30 minutes; 59 ± 8 mmHg vs. 51 ± 5 mmHg at 3 hours post-ECMO) and cardiac function (shortening fraction: 60 ± 16% vs. 42 ± 8%; P = 0.01). Additionally, the aptamer group exhibited better platelet preservation (platelet count decrease: -288,000 ± 121,000/μL vs. -404,000 ± 89,000/μL; P = 0.03). Inflammatory profiles were similar between groups, except for a transient increase in interleukins 10 (IL-10) in the aptamer group. Histopathological analysis revealed no significant differences in myocardial lesions.</p><p><strong>Conclusions: </strong>The antidote-controlled anti-FIXa aptamer represents an alternative anticoagulant strategy that may prove useful for managing patients with a history of heparin-induced thrombocytopenia (HIT) and myocardial dysfunction associated with protamine administration.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 2","pages":"87-98"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing mRNA technology for ischemic heart disease: a review of regenerative and protective therapies.","authors":"Matthew Adjmi, Isabelle Tse, Lior Zangi","doi":"10.1097/CP9.0000000000000118","DOIUrl":"10.1097/CP9.0000000000000118","url":null,"abstract":"<p><p>As ischemic heart disease (IHD) remains the leading cause of mortality worldwide, there is an urgent need for innovative therapies that go beyond symptom management. The irreversible damage to cardiac tissue following myocardial infarction (MI) and the limited regenerative and proliferative capacity of adult cardiomyocytes (CMs) present significant challenges to the development of treatments capable of restoring cardiac function. This review focuses on emerging modified and non-modified messenger ribonucleic acid (mRNA)-based therapies, which offer targeted and transient protein expression. The studies reviewed here address three major therapeutic strategies: cardiac regeneration, aimed at inducing CM proliferation to restore lost cardiac muscle; cardiac protection, centered on anti-apoptotic and anti-inflammatory methods to mitigate further tissue damage; and cardiovascular regeneration, focused on promoting angiogenesis and restoring vascular integrity after injury. By examining mRNA and modified mRNA (modRNA) therapies across these three approaches, this review showcases mRNA's promising role in advancing muscular and vascular regenerative and protective therapeutics for IHD.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 2","pages":"117-128"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cepharanthine aggravated atherosclerosis and liver injury in Apoe −/− and Ldlr −/− mice","authors":"Fanshun Zhang, Yanjun Yin, Jianping Weng, Suowen Xu","doi":"10.1097/cp9.0000000000000109","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000109","url":null,"abstract":"Background and purpose: Cepharanthine, an alkaloid purified from the earthnut Stephania Epigaea, exhibits antitumor, anti-inflammatory, and immunomodulatory effects. During the coronavirus disease 2019 (COVID-19) epidemic, cepharanthine was identified to restrain severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and reduced the inflammatory response. Viral infections, which disrupt internal homeostasis, often exacerbate atherosclerosis, contributing to cardiovascular complications. Based on the antiviral and anti-inflammatory efficacy of cepharanthine and the recognition of atherosclerosis as a chronic inflammatory disease, this study aimed to evaluate whether cepharanthine could attenuate atherogenesis in two established mouse models of atherosclerosis. Methods: Atherosclerosis was induced in Apoe −/− and Ldlr −/− mice through feeding with a high-fat and high-cholesterol diet. Mice were administered 20 mg/kg cepharanthine daily for 8 weeks. Atherosclerotic lesions in the aorta and aortic sinus were evaluated using Oil Red O staining. Liver tissues were analyzed for liver injury and fibrosis using hematoxylin and eosin (H&amp;E) and Sirius Red staining. Results: Contrary to expectations, cepharanthine aggravated atherosclerosis in both Apoe −/− and Ldlr −/− mice. Treated mice exhibited significant liver injury, characterized by hepatocyte swelling and fibrosis, with increased collagen deposition and the increased expression of Vimentin. Cepharanthine also decreased hepatic Abcg5 expression while upregulating Fabp4 expression. Elevated serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels indicated worsened liver and heart injury in cepharanthine-treated mice. Conclusions: This study highlights potential safety concerns with cepharanthine especially for patients with hyperlipidemia, atherosclerosis, and COVID-19. These findings underscore the need for careful monitoring of its clinical use.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"10 1","pages":"23-33"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}