Cardiovascular Research最新文献

{"title":"Sweeteners: erythritol, xylitol and cardiovascular risk - friend or foe?","authors":"Bettina K Wölnerhanssen, Anne Christin Meyer-Gerspach, Arduino Arduini, Angelo D’Alessandro, Edoardo Gronda, Stefano Carugo, Mario Bonomini, Maurizio Gallieni, Valentina Masola, Anne Angelillo-Scherrer, Tommaso Prosdocimi, Gary D Lopaschuk","doi":"10.1093/cvr/cvaf091","DOIUrl":"https://doi.org/10.1093/cvr/cvaf091","url":null,"abstract":"Hyperglycemia harms vascular health and promotes platelet aggregation. Reducing glucose concentration is crucial, and sugar alcohols may aid this effort. Used for over 50 years in food, cosmetic, and pharmaceutical industries, erythritol and xylitol minimally affect plasma glucose and insulin levels while promoting the release of beneficial gastrointestinal hormones such as e.g. glucagon-like peptide-1 (GLP-1). These properties make them particularly appealing for individuals with diabetes, obesity, and metabolic syndrome. Recent pilot trials suggest that xylitol and erythritol might temporarily alter platelet aggregation. Studies on critically ill patients receiving large intravenous doses and Mendelian randomization trials do not link sugar alcohols to significant cardiovascular risks. Sugar alcohols are also endogenously produced in the body, and while their increased production under certain conditions is not fully understood, it requires further research. This review discusses the physiology and metabolism of erythritol and xylitol, and other sugar alcohols, their roles in metabolomic profiling, effects on platelet aggregation and cardiovascular risk, related genetic disorders, vascular impacts, and usage in critically ill patients.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"35 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRDM16, a new kid on the block in cardiovascular health and disease.","authors":"Jore Van Wauwe, Hannelore Kemps, Pieter Vrancaert, Alexia Mahy, Robin Schellingen, Mandy O J Grootaert, Manu Beerens, Aernout Luttun","doi":"10.1093/cvr/cvaf089","DOIUrl":"https://doi.org/10.1093/cvr/cvaf089","url":null,"abstract":"<p><p>Transcriptional regulation is essential for the development, homeostasis, and function of all organisms. Transcription factors and epigenetic modifiers play an indispensable role by direct or indirect interaction with DNA or chromatin. Although the role of transcription factor PRDM16 in adipose, hematopoietic, skeletal, and neural cell lineage specification is well-documented, its function within the cardiovascular system has only recently gained significant attention. Similar as in adipose tissue, PRDM16 displays an asymmetric expression pattern within the cardiovascular system, where it is exclusively expressed by ventricular cardiomyocytes and endothelial and smooth muscle cells of arteries, while being absent in their atrial and venous counterparts. Concordantly, an increasing number of clinical and preclinical studies have identified PRDM16 as an important multi-modal regulator of cardiovascular development and function. Moreover, aberrant PRDM16 expression has now been linked to (cardio)vascular diseases, including left ventricular non-compaction, migraine, and coronary artery disease. In this review, we give a synopsis of PRDM16's expression and function within (developing) cardiovascular tissues and provide insights into how impaired PRDM16 signaling contributes to cardiovascular disease.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted delivery of TAPI-1 via biomimetic nanoparticles ameliorates post-infarct left ventricle function and remodelling.","authors":"Qing Chen, Yang Yu, Lei Tong, Robert M Weiss, Shun-Guang Wei","doi":"10.1093/cvr/cvaf039","DOIUrl":"10.1093/cvr/cvaf039","url":null,"abstract":"<p><strong>Aims: </strong>The potential of nanoparticles as effective drug delivery tools for treating failing hearts in heart failure remains a challenge. Leveraging the rapid infiltration of neutrophils into infarcted hearts after myocardial infarction (MI), we developed a nanoparticle platform engineered with neutrophil membrane proteins for the targeted delivery of TAPI-1, a TACE/ADAM17 inhibitor, to the inflamed myocardium, aiming to treat cardiac dysfunction and remodelling in rats with MI.</p><p><strong>Methods and results: </strong>Neutrophil-mimic liposomal nanoparticles (Neu-LNPs) were constructed by integrating synthesized liposomal nanoparticles with LPS-stimulated neutrophil membrane fragments and then loaded with TAPI-1. MI rats were treated with TAPI-1 delivered via Neu-LNPs for 4 weeks. Left ventricular function was assessed by echocardiography and cardiac fibrosis was evaluated post-treatment. The novel Neu-LNPs maintained typical nanoparticle features, but with increased biocompatibility. Neu-LNPs demonstrated improved targeting ability and cellular internalization, facilitated by LFA1/Mac1/ICAM-1 interaction. Neu-LNPs displayed higher accumulation and cellular uptake by macrophages and cardiomyocytes in infarcted hearts post-MI, with a sustained duration. Treatments with TAPI-1-Neu-LNPs demonstrated greater protection against myocardial injury and cardiac dysfunction in MI rats compared to untargeted TAPI-1, along with reduced cardiac collagen deposition and expression of fibrosis biomarkers as well as altered immune cell compositions within the hearts.</p><p><strong>Conclusions: </strong>Targeted treatment with TACE/ADAM17 inhibitor delivered via biomimetic nanoparticles exhibited pronounced advantages in improving left ventricle function, mitigating cardiac remodelling, and reducing inflammatory responses within the infarcted hearts. This study underscores the effectiveness of Neu-LNPs as a drug delivery strategy to enhance therapeutic efficacy in clinical settings.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"760-774"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-ischaemic empagliflozin treatment attenuates blood-brain barrier disruption via β-catenin mediated protection of cerebral endothelial cells.","authors":"Guohao Liu, Yanmei Qiu, Nanlin You, Mengchen Yu, Wenbo Chen, Tao Sun, Zhen Qin, Mengtao Han, Zhiwei Xue, Xiangjun Liang, Bo Mao, Lu Ling, Yanzhao Wu, Wenchen Xing, Quanmeng Liu, Donghai Wang","doi":"10.1093/cvr/cvaf026","DOIUrl":"10.1093/cvr/cvaf026","url":null,"abstract":"<p><strong>Aims: </strong>Microvascular endothelial cells dysfunction can significantly worsen ischaemic stroke outcomes by disrupting tight junctions and increasing the acquisition of adhesion molecules, accelerating blood-brain barrier (BBB) disruption and pro-inflammatory response. The identification of drugs that improve endothelial cell function may be crucial for ischaemic stroke. It has been validated that empagliflozin (EMPA), a novel antidiabetic drug, protects endothelial cells regardless of the diabetic status of the patient. However, the impact of EMPA on stroke outcomes is unclear. We hypothesized that EMPA would exert a beneficial effect on ischaemic stroke outcome by protecting microvascular endothelial cells against tight junction disruption and the increase of adhesion molecules.</p><p><strong>Methods and results: </strong>Young adult male mice were administered with EMPA or vehicle (dimethyl sulfoxide) daily for 7 days before being subjected to transient middle cerebral artery occlusion (tMCAO). Neurological deficits were evaluated for up to 28 days post-tMCAO. Infarct volume, BBB disruption, and inflammatory status were assessed 1 day after tMCAO.bEnd.3 cells and primary brain microvascular endothelial cells were treated with EMPA or vehicle under oxygen and glucose deprivation/reperfusion (OGD/R), and the lactate dehydrogenase release, transendothelial electrical resistance, leakage of fluorescein isothiocyanate-dextran, and tight junction and adhesion molecules proteins were examined. Mechanistic studies probing the effect of EMPA on endothelial cells were conducted by RNA-seq. EMPA treatment before ischaemia markedly improved infarct volume, BBB disruption, and inflammation 1-day post-tMCAO, and further enhanced neurobehavioral function up to 28 days. Pre-treatment of EMPA attenuated endothelial cell dysfunction under OGD/R conditions. In mechanistic terms, RNA-seq data from isolated cerebral microvessels revealed that the Wnt/β-catenin signalling pathway was preserved in the EMPA group, in contrast to the vehicle group. Pre-treatment with EMPA inhibited β-catenin ubiquitination and promoted β-catenin translocation from the cytoplasm to the nucleus to improve endothelial cell function. Importantly, the β-catenin inhibitor XAV-939 eliminated this protective function of EMPA.</p><p><strong>Conclusion: </strong>EMPA administration before tMCAO attenuated ischaemia/reperfusion-induced BBB disruption and inflammation via β-catenin-mediated protection of cerebral microvascular endothelial cells. Therefore, EMPA shows potential for improving stroke outcomes as an adjunctive preventive strategy.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"788-802"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From mice to humans: advancing the path to cardioprotection.","authors":"Lina Badimon, Gemma Vilahur, Guiomar Mendieta","doi":"10.1093/cvr/cvaf048","DOIUrl":"10.1093/cvr/cvaf048","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"692-693"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A paradigm shift in cardiovascular research: new method isolates intestinal interstitial fluid to understand gut microbiome and host cross-talk.","authors":"Fadi J Charchar, Francine Z Marques","doi":"10.1093/cvr/cvaf047","DOIUrl":"10.1093/cvr/cvaf047","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"697-698"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin 1-7 and a telomerase reverse transcriptase activator individually restore vasodilatory capacity within the human microcirculation previous SARS-CoV-2 infection.","authors":"Yoshinori Nishijima, Shelby N Hader, Erin C Birch, Yiliang Chen, Michael E Widlansky, Andreas M Beyer","doi":"10.1093/cvr/cvaf020","DOIUrl":"10.1093/cvr/cvaf020","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"699-701"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial c-REL orchestrates atherosclerosis at regions of disturbed flow through crosstalk with TXNIP-p38 and non-canonical NF-κB pathways.","authors":"Blanca Tardajos Ayllon, Neil Bowden, Celine Souilhol, Hazem Darwish, Siyu Tian, Carrie Duckworth, David Mark Pritchard, Suowen Xu, Jon Sayers, Sheila Francis, Jovana Serbanovic-Canic, Fiona Oakley, Paul Charles Evans","doi":"10.1093/cvr/cvaf024","DOIUrl":"10.1093/cvr/cvaf024","url":null,"abstract":"<p><strong>Aims: </strong>Atherosclerosis initiation at sites of disturbed blood flow involves heightened inflammation coupled to excessive endothelial cell (EC) proliferation. Here, we unveil the pivotal role of c-REL, a member of the NF-κB transcription factor family, in orchestrating these processes by driving dual pathological inflammatory and cell cycle pathways.</p><p><strong>Methods and results: </strong>Analysis of cultured EC and murine models revealed enrichment and activation of c-REL at atherosusceptible sites experiencing disturbed flow. Transcriptome analysis, extensively validated in vitro and in vivo, demonstrates that endothelial c-REL drives inflammation via a TXNIP-p38 MAP kinase signalling pathway and enhances proliferation through a non-canonical NFKB2-p21 pathway. Consistent with its pivotal role in EC pathology, genetic deletion of c-Rel in EC significantly reduces plaque burden in hypercholesterolaemic mice.</p><p><strong>Conclusion: </strong>These findings underscore the fundamental role of c-REL in endothelial responses to disturbed flow and highlight therapeutic targeting of endothelial c-REL as a potential strategy for atherosclerosis treatment.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"748-759"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mimicked immunity: a strategy for targeted nanodrug delivery.","authors":"Yapei Zhang, Charles C Hong, Bryan Ronain Smith","doi":"10.1093/cvr/cvaf050","DOIUrl":"10.1093/cvr/cvaf050","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"690-691"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Keep your guard up: blood-brain barrier protection by empagliflozin after acute ischaemic stroke.","authors":"Karin Hochrainer, Ashley Hansen, Lidia Garcia-Bonilla","doi":"10.1093/cvr/cvaf049","DOIUrl":"10.1093/cvr/cvaf049","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"694-696"},"PeriodicalIF":10.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}