Cardiovascular Research最新文献

{"title":"Let food be thy medicine: anti-inflammatory diets and the hidden properties of coronary plaque.","authors":"Eiry Jones,Tomasz J Guzik","doi":"10.1093/cvr/cvaf115","DOIUrl":"https://doi.org/10.1093/cvr/cvaf115","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"109 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640091","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":"Prevalence of hypertension in Africa in the last two decades: Systematic review and meta-analysis.","authors":"Paul Olowoyo,Akinkunmi Paul Okekunle,Osahon Jeffery Asowata,Segun Atolani,Moustafa I Morsy,Elisabetta Caiazzo,Bamba Gaye,David Danladi Kadan,Dario Bruzzese,Tomasz J Guzik,Pasquale Maffia,Mayowa O Owolabi","doi":"10.1093/cvr/cvaf125","DOIUrl":"https://doi.org/10.1093/cvr/cvaf125","url":null,"abstract":"AIMSDespite being the most common cardiovascular risk factor, the actual burden of hypertension is poorly characterized in Africa. We meta-analyzed the most extensive pooled data to determine the overall prevalence of hypertension in Africa.METHODS AND RESULTSFollowing PRISMA guidelines, we systematically searched Google Scholar, PubMed, ScienceDirect, and Web of Science databases to retrieve prevalence studies only on hypertension among Africans published between 2002 and 2023. Furthermore, we meta-analyzed the crude and age-adjusted prevalences of hypertension using a random effect model due to the expected high heterogeneity, with logit transformation of the original proportions.Seventy-eight (out of an initial 779 screened) articles with complete data were included, with a total number of hypertension cases of 71,004 and a denominator population of 286,575, mostly from community-based studies in 23 countries. The pooled crude prevalence of hypertension was 28⸱5/100 persons [95% confidence interval (CI): 25⸱3%-31⸱8%] and a 95% prediction interval of 7⸱6%-65⸱6%; the pooled prevalence increased with age and was highest among the aged ≥75 years: 51⸱4% (95%CI: 42⸱0%-60⸱6%) and remained highest in the Southern Africa region overall (34⸱8%) and in the last decade (2013-2023; 44⸱5%). The point estimate of the pooled crude prevalence was higher among urban dwellers, 32⸱9% (95%CI: 26⸱8%-39⸱5%), than rural residents, 26⸱3% (95%CI: 20⸱4%-33⸱3%). In a subset of twenty-one articles reporting age stratification consistent with the WHO standard population, the pooled age-standardized prevalence was 27⸱2/100 persons (95%CI: 20⸱9%-33⸱6%).CONCLUSIONThe burden of hypertension remains high, especially in urban areas and with increasing age. Frequent screening and treatment are recommended, especially in urban areas.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"35 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144630258","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":"Sirtuin-1 directly binds and deacetylates hepatic PCSK9 thereby promoting the inhibition of LDL receptor degradation.","authors":"Srividya Velagapudi,Melroy X Miranda,Priyanka Adla,Simon Kraler,Shafeeq A Mohammed,Shekhar Baki,Jerome Robert,Lucia Rohrer,Hwan Lee,Hyun-Duk Jang,Slayman Obeid,Anne Tailleux,Bart Staels,Naresh Babu V Sepuri,Francesco Paneni,Ravi Kumar Gutti,Arnold von Eckardstein,Hyo-Soo Kim,Alexander Akhmedov,Giovanni G Camici,Thomas F Lüscher","doi":"10.1093/cvr/cvaf087","DOIUrl":"https://doi.org/10.1093/cvr/cvaf087","url":null,"abstract":"AIMSLow-density lipoprotein (LDL)-cholesterol is causally involved in atherosclerotic cardiovascular disease (ASCVD) pathogenesis. Pharmacological activation of the intracellular NAD + -dependent deacetylase Sirtuin-1 (SIRT1) reduces plasma LDL-cholesterol levels by increasing hepatic LDL-receptor (LDLR) expression, which intriguingly associates with atheroprotective effects. Recent studies have identified the presence of SIRT1 in plasma, however, its effects remain elusive. We found that plasma levels of SIRT1 to be decreased in atherosclerotic mice compared with wild-type controls and aimed to investigate the therapeutic potential of systemic SIRT1 restoration on lipid metabolism and plaque burden in atherosclerotic mice and dissect the underlying molecular mechanisms involved.METHODS AND RESULTSTwelve-week-old apolipoprotein E-deficient (ApoE-/-) mice fed a high-cholesterol diet (1.25% w/w) were randomized to receive recombinant murine SIRT1(rmSIRT1) (n = 6; 0.3 mg/kg BW i.p.) or vehicle (n = 6; PBS) every third day over 4 weeks. Boosting systemic SIRT1 levels increased hepatic LDLR protein expression, reduced plasma LDL-cholesterol levels and decreased plaque progression in ApoE-/- mice. Yet, rmSIRT1 treatment did not change hepatic proprotein convertase subtilisin/kexin type 9 (PCSK9) expression but notably increased its deacetylated levels. Mechanistically, rmSirt1 directly bound to hepatic PCSK9 thereby promoting PCSK9 deacetylation involving 3 sites, namely Lys243, Lys421, and Lys506, as shown by mass spectrometric analyses. In vitro mutagenesis to triple deacetylation mimetic (3KR) reduced SIRT1-induced PCSK9 activity, as evidenced by increased cellular binding and association of 125I-LDL to hepatic LDLR. Finally, plasma levels of SIRT1 and PCSK9 were assessed at baseline in patients with acute coronary syndromes. In these patients, plasma SIRT1 levels correlated inversely with PCSK9 with high SIRT1 levels conferring a reduced risk of major adverse cardiovascular events (MACE).CONCLUSIONSIRT1 directly binds hepatic PCSK9 and decreases its activity by deacetylation, thereby enhancing LDL-cholesterol clearance by hepatic LDLR upregulation. Boosting circulating SIRT1 exerts atheroprotective effects in mice, with high levels associating with improved prognosis in patients with established ASCVD.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"19 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144622141","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":"Right stellate ganglion stimulation modulates arrhythmogenesis in acute left lateral ventricular ischemia","authors":"Joseph E Hadaya, Bastiaan J D Boukens, Michiel J Janse, Steven Cha, Al-Hassan Dajani, Ronald Challita, Ruben Coronel, Jeffrey L Ardell, Kalyanam Shivkumar, Veronique M F Meijborg","doi":"10.1093/cvr/cvaf121","DOIUrl":"https://doi.org/10.1093/cvr/cvaf121","url":null,"abstract":"Aim Acute myocardial ischemia causes fatal arrhythmias as result of a flow of ‘injury current’. Left stellate ganglion stimulation (LSGS) modulates the injury current and is arrhythmogenic during left anterior ventricular wall ischemia. The role of right stellate ganglion stimulation (RSGS) in arrhythmogenesis is unclear. We hypothesized, that RSGS is proarrhythmic during left lateral ventricular wall ischemia. Methods and results In 11 anesthetized female pigs, ventricular repolarization was measured in unipolar epicardial electrograms from the left lateral ventricular wall. Seven subsequent episodes of acute ischemia (5 minutes) were produced by occlusion of the circumflex coronary artery (CX), separated by 20 minutes of reperfusion. The second occlusion served as a control. After 3 minutes of ischemia during the third occlusion, LSGS was initiated for 30 seconds. In the 4th occlusion, RSGS was performed. After decentralization of both left and right stellate ganglia and vagal nerves, LSGS and RSGS were initiated (6th and 7th occlusion). RSGS during ischemia was more arrhythmogenic than LSGS or control with more spontaneous ventricular premature beats (3-5 minutes of ischemia) and 2 instances of ventricular fibrillation. The LSGS-induced effect on repolarization was absent in myocardium that had been ischemic for 3 minutes by CX occlusion. Conclusions LSGS-induced repolarization shortening is absent in ischemic myocardium. RSGS was more arrhythmogenic following CX-occlusion than LSGS or control. These data demonstrate that the arrhythmogenic influence of RSGS or LSGS is contingent on the location of ischemic zone supporting the clinical findings that bilateral sympathectomy is superior to left sympathectomy alone.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"15 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629886","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":"C-C Motif chemokine receptor-2 blockade ameliorates pulmonary hypertension in rats and synergizes with a pulmonary vasodilator.","authors":"Naoki Tsuboya, Hirofumi Sawada, Yoshihide Mitani, Hironori Oshita, Kazunobu Ohya, Mami Takeoka, Jane Chanda Kabwe, Yoshiki Miyasaka, Hiromasa Ito, Noriko Yodoya, Hiroyuki Ohashi, Junko Maruyama, Ryuji Okamoto, Tomoji Mashimo, Kaoru Dohi, Yuhei Nishimura, Kazuo Maruyama, Masahiro Hirayama","doi":"10.1093/cvr/cvae244","DOIUrl":"10.1093/cvr/cvae244","url":null,"abstract":"<p><strong>Aims: </strong>We investigated whether the disruption of C-C motif chemokine receptor (CCR) 2 may attenuate the development of pulmonary arterial hypertension (PAH) in any rat models with the reversal of the associated pro-inflammatory state and vascular dysfunction, and synergize with a conventional pulmonary vasodilator.</p><p><strong>Methods and results: </strong>Using Ccr2(-/-) rats generated by CRISPR/Cas9, we investigated pulmonary hypertension (PH) in Ccr2(+/+) or Ccr2(-/-) rats treated with monocrotaline (MCT), SU5416/hypoxia (SuHx) and chronic hypoxia (CH). Ccr2(-/-) decreased the right ventricular systolic pressure, an index of right ventricular hypertrophy and mortality rate, and reversed increased expression of inflammatory cytokines/chemokines [interleukin-6, tumour necrosis factor-α, C-C motif chemokine receptor (CCL)-2, interleukin-1β, transforming growth factor-β] in rats 3weeks after MCT injection, but not in SuHx or CH models. Consistently, Ccr2(-/-) decreased indices of pulmonary vascular diseases (PVDs) and perivascular macrophage infiltration, as well as reversed impaired bone morphogenetic protein receptor type 2 signalling, increased endothelial apoptosis and impaired nitric oxide signalling and decreased phosphodiesterase-5 (PDE5) expression in lungs in MCT-treated rats. Gene expression of receptors for prostaglandin I2 and endothelin was not changed by Ccr2(-/-) in MCT-treated rats. In cultured pulmonary arterial smooth muscle cells (PASMCs), Ccr2(-/-) suppressed CCL2-induced hyperproliferation and dedifferentiation as well as reversed CCL2-induced decrease in PDE5 expression. The whole-genome RNA sequencing analysis identified differentially expressed genes in CCL2-stimulated Ccr2(-/-) PASMCs, which are related to the regulation of cellular differentiation and contraction. Based on studies in rats and cultured PASMCs, we investigated whether a PDE5 inhibitor, tadalafil, synergizes with Ccr2(-/-). Tadalafil administration ameliorated PH and PVDs in MCT-treated Ccr2(-/-) rats but not in Ccr2(+/+) rats. Tadalafil further improved survival in MCT-treated Ccr2(-/-) rats.</p><p><strong>Conclusion: </strong>The present findings demonstrated that CCR2 disruption ameliorated PAH in MCT-treated rats, which was associated with the reversal of dysregulated inflammatory pathways and vascular dysfunction and synergized with tadalafil. These findings suggest that CCR2 may be a therapeutic target in intractable PAH patients with a certain CCR2-related inflammatory phenotype and refractory to conventional pulmonary vasodilators.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1076-1090"},"PeriodicalIF":10.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236072/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646878","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":"Endothelial insulin-like growth factor-1 signalling regulates vascular barrier function and atherogenesis.","authors":"Michael Drozd, Alexander-Francisco Bruns, Nadira Y Yuldasheva, Azhar Maqbool, Hema Viswambharan, Anna Skromna, Natallia Makava, Chew W Cheng, Piruthivi Sukumar, Lauren Eades, Andrew M N Walker, Kathryn J Griffin, Stacey Galloway, Nicole T Watt, Natalie Haywood, Victoria Palin, Nele Warmke, Helen Imrie, Katherine Bridge, David J Beech, Stephen B Wheatcroft, Mark T Kearney, Richard M Cubbon","doi":"10.1093/cvr/cvaf055","DOIUrl":"10.1093/cvr/cvaf055","url":null,"abstract":"<p><strong>Aims: </strong>Progressive deposition of cholesterol in the arterial wall characterizes atherosclerosis, which underpins most cases of myocardial infarction and stroke. Insulin-like growth factor-1 (IGF-1) is a hormone that regulates systemic growth and metabolism and possesses anti-atherosclerotic properties. We asked whether endothelial-restricted augmentation of IGF-1 signalling is sufficient to suppress atherogenesis.</p><p><strong>Methods and results: </strong>We generated mice with endothelial-restricted over-expression of human wild-type (WT) IGF-1R (hIGFREO/ApoE-/-) or a signalling-defective K1003R mutant human IGF-1R (mIGFREO/ApoE-/-) and compared them with their respective ApoE-/- littermates. hIGFREO/ApoE-/- had less atherosclerosis, circulating leucocytes, arterial cholesterol uptake, and vascular leakage in multiple organs, whereas mIGFREO/ApoE-/- did not exhibit these phenomena. Over-expressing WT IGF-1R in human umbilical vein endothelial cells (HUVECs) altered the localization of tight junction proteins and reduced paracellular leakage across their monolayers, whilst over-expression of K1003R IGF-1R did not have these effects. Moreover, only over-expression of WT IGF-1R reduced HUVEC internalization of cholesterol-rich low-density lipoprotein particles and increased their association of these particles with clathrin, but not caveolin-1, implicating it in vesicular uptake of lipoproteins. Endothelial over-expression of WT vs. K1003R IGF-1R also reduced expression of YAP/TAZ target genes and nuclear localization of TAZ, which may be relevant to its impact on vascular barrier and atherogenesis.</p><p><strong>Conclusion: </strong>Endothelial IGF-1 signalling modulates both para- and transcellular vascular barrier function. Beyond reducing atherosclerosis, this could have relevance to many diseases associated with abnormal vascular permeability.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1108-1120"},"PeriodicalIF":10.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762736","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":"Emerging role of Cellular communication network factor 2 as a guardian of smooth muscle cell phenotype and vascular integrity.","authors":"Jannik Hjortshøj Larsen, Lasse Bach Steffensen","doi":"10.1093/cvr/cvaf015","DOIUrl":"10.1093/cvr/cvaf015","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"985-987"},"PeriodicalIF":10.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390376","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":"C-C motif chemokine receptor 2 and phosphodiesterase type 5 inhibition in immune subphenotypes: a step toward personalized treatment for pulmonary arterial hypertension?","authors":"Christian J Goossen, Patrick J Pagano","doi":"10.1093/cvr/cvaf081","DOIUrl":"10.1093/cvr/cvaf081","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"980-982"},"PeriodicalIF":10.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257431","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":"Platelet derived RNAs: a new regulatory marker for vascular inflammation?","authors":"Shinya Goto,Masayuki Oki,Shinichi Goto","doi":"10.1093/cvr/cvaf124","DOIUrl":"https://doi.org/10.1093/cvr/cvaf124","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"21 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568439","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":"GATA5/ISL1+ fibroblasts: the hidden architects of cardiac repair.","authors":"Sauri Hernandez-Resendiz, Elisa A Liehn, Derek J Hausenloy","doi":"10.1093/cvr/cvaf123","DOIUrl":"https://doi.org/10.1093/cvr/cvaf123","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559308","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}