Vascular pharmacology最新文献

{"title":"Translational aspects of doxorubicin-induced cardiotoxicity: What we have omitted for the past decades?","authors":"Ashot Avagimyan ,&nbsp;Rosalinda Madonna ,&nbsp;Mohammad Sheibani ,&nbsp;Nana Pogosova ,&nbsp;Artem Trofimenko ,&nbsp;Olga Urazova ,&nbsp;Laura Iop ,&nbsp;Zinaida Jndoyan ,&nbsp;Hasmik Yeranosyan ,&nbsp;Anahit Aznauryan ,&nbsp;Karmen Sahakyan ,&nbsp;Anna Petrosyan ,&nbsp;Ruzanna Petrosyan ,&nbsp;Marina Tatoyan ,&nbsp;Gayane Mkrtchyan ,&nbsp;Elina Sulemaniayants ,&nbsp;Goarik Meltonyan ,&nbsp;Aleh Kuzniatsou ,&nbsp;Rupak Mukherjee ,&nbsp;Aysa Rezabakhsh ,&nbsp;Nizal Sarrafzadegan","doi":"10.1016/j.vph.2025.107526","DOIUrl":"10.1016/j.vph.2025.107526","url":null,"abstract":"<div><div>Anthracyclines remain the cornerstone of treatment for malignancies with dose-dependent cardiac damage, ranging from oxidative stress and mitochondrial dysfunction to DNA damage and ferroptosis, and continue to compromise patient outcome.</div><div>Animal models, encompassing rodents, rabbits, pigs, and nonhuman primates, are essential for investigating doxorubicin (DOX)-induced cardiovascular toxicity. Acute models facilitate rapid evaluation of cardiac injury; however, they frequently fail to replicate chronic human cardiomyopathy. In contrast, chronic models represent clinical scenarios more accurately but encounter logistical challenges. Species-specific variations in drug metabolism, cardiac physiology, and compensatory mechanisms further complicate the extrapolation. The primary limitations of existing models include the absence of comorbid conditions, lack of combination chemotherapy protocols, and underrepresentation of sex- and age-specific responses. Addressing these challenges is crucial for the development of effective and personalized cardioprotective strategies in cardio-oncology.</div><div>This review explores the translational challenges of DOX-induced cardiotoxicity, a critical limitation in the development of new cardioprotective strategies in cardio-oncology despite decades of research. We will elucidate the underlying factors that contribute to the difficulties in translating experimental in vivo results into clinical applications.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107526"},"PeriodicalIF":3.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144711467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring new cardiovascular frontiers: The Italian cardiovascular research landscape.","authors":"Rosalinda Madonna, Vincenzo Lionetti","doi":"10.1016/j.vph.2025.107525","DOIUrl":"10.1016/j.vph.2025.107525","url":null,"abstract":"","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":" ","pages":"107525"},"PeriodicalIF":3.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144709174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antagonism of the complement receptor reduces oxidative stress and matrix metalloproteinase (MMP)-2 activity in the aortas of mice with angiotensin-II-induced hypertension","authors":"Luan Victor Resque Ramos,&nbsp;Marcela M. Blascke de Mello,&nbsp;Bruno Marcel Silva de Melo,&nbsp;José Teles de Oliveira Neto,&nbsp;Evellin Karina Pires Bueno,&nbsp;José Carlos Farias Alves Filho,&nbsp;Rita Tostes,&nbsp;Michele M. Castro","doi":"10.1016/j.vph.2025.107523","DOIUrl":"10.1016/j.vph.2025.107523","url":null,"abstract":"<div><div>Angiotensin II (Ang II) increases C3a effects through its receptors, promoting aortic oxidative stress and upregulating matrix metalloproteinase (MMP)-2. MMP-2 is implicated in hypertrophic arterial remodeling in hypertension. This study investigated whether C3a receptor activation contributes to oxidative stress and increased MMP-2 activity in aortas of Ang II treated mice, ultimately leading to maladaptive vascular changes. Hypertension was induced in C57BL/6 mice via subcutaneous implantation of osmotic mini pumps delivering Ang II (1000 ng/kg/min) for 14 days. Mice were administered the C3aR antagonist, SB290157 (1 mg/kg/day, intraperitoneally) every other day for 14 days. Systolic blood pressure (SBP) and vascular function were assessed via direct blood pressure measurements and contraction and relaxation analysis in a wire myography. Aortic MMP-2 activity was analyzed by gel and in situ zymography. SB290157 did not decrease SBP, aortic hypertrophy or increased aortic reactivity to phenylephrine in Ang II treated mice. Ang II exhibited higher levels of C3a in the plasma and increased tumor necrose factor (TNF)-α and interleukin (IL)-6 in the kidneys (*<em>p</em> &lt; 0.05). SB290157 did not alter C3a, but reduced TNF-α and IL-6 in hypertension (#<em>p</em> &lt; 0.05 vs. Ang II). SB290157 also decreased aortic oxidative stress and p65 factor nuclear kappa B (NFkB) in Ang II treated mice (*<em>p</em> &lt; 0.05). MMP-2 activity was increased in the aortas of Ang II (*<em>p</em> &lt; 0.05) and SB290157 decreased it (*<em>p</em> &lt; 0.05). Pharmacological antagonism of C3a receptor attenuates oxidative stress and MMP-2 activity in the aortas of Ang II treated mice.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107523"},"PeriodicalIF":3.5,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual L/T calcium channel blocker exerts both antihypertensive and renoprotective effects in L-NAME-induced hypertension model","authors":"Peter Muiruri Kamau ,&nbsp;Yang Chen ,&nbsp;Xiaopei Yang ,&nbsp;Jinglin Li ,&nbsp;Rebecca Caroline Thuku ,&nbsp;Dawit Tadese ,&nbsp;Hao Zhang ,&nbsp;Haiying Wu ,&nbsp;Lei Luo ,&nbsp;Qiumin Lu","doi":"10.1016/j.vph.2025.107524","DOIUrl":"10.1016/j.vph.2025.107524","url":null,"abstract":"<div><div>Renal hypertension, a common form of secondary hypertension, results from kidney disease. It arises due to the narrowing of arteries connected to the kidneys, often caused by atherosclerosis. Over time, this condition can lead to kidney failure. Therapeutics for kidney protection are currently limited, prompting continual search for new renoprotective agents in the context of hypertension. Dual blockage of both L-type and T-type calcium channels has shown promise in the treatment of hypertension when compared to selective calcium channel blockers. Toddaculin has been proven to be a potent inhibitor of the T-type channel. Conserved amino acid sequence comparison, electrophysiological recordings, and Flex Station were used to evaluate and compare toddaculin effect on the Ca_V3.1 and Ca_V1.2 channels and their respective residues, transiently expressed in HEK293T cells. Intracellular Ca²⁺ was assessed using the molecular probe fluo-4-AM. They specifically investigated the impact of toddaculin on vascular smooth muscle cells (VSMCs). Toddaculin's myogenic effects were assessed using aortic rings isolated from rats within an organ bath system. In an in vivo context, a mouse model with L-NAME-induced hypertension was employed to investigate toddaculin's anti-hypertensive and renoprotective properties. We found that L1047A in Ca_V1.2, and L1456A in Ca_V3.1 are potential key binding sites for toddaculin, and that toddaculin inhibited Ca_V3.1 and Ca_V1.2 equally and dose-dependently. Toddaculin-induced decline of [Ca²⁺]_i cultured VSMCs under a laser scanning confocal microscopy. Aortic rings exposed to toddaculin demonstrated dose-dependent relaxation following KCl-induced contraction. Moreover, toddaculin exhibited significant blood pressure reduction and renoprotective effects against L-NAME-induced renal injury in mice. This finding provides an evident therapeutic potential of toddaculin as an antihypertensive drug candidate with a renoprotective effect.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107524"},"PeriodicalIF":3.5,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in circulating lipopolysaccharide and zonulin following acute myocardial infarction: The impact of smoking","authors":"Rafał Kolec ,&nbsp;Michał Słaboszewski ,&nbsp;Elżbieta Paszek ,&nbsp;Mateusz Baran ,&nbsp;Anetta Undas","doi":"10.1016/j.vph.2025.107522","DOIUrl":"10.1016/j.vph.2025.107522","url":null,"abstract":"<div><h3>Background</h3><div>Serum lipopolysaccharide (LPS), a marker of gut dysbiosis and endotoxemia is associated with myocardial infarction (MI). We investigated factors affecting LPS changes in MI patients treated with percutaneous coronary intervention (PCI) and aimed to establish factors associated with the degree of LPS decrease following MI.</div></div><div><h3>Methods</h3><div>In 46 PCI-treated MI patients (mean age 57.2 [8.6]) years we measured LPS and zonulin, a marker of gut permeability, on admission, 30 and 60 days thereafter, inflammatory markers (interleukin [IL]-6, IL-18), P-selectin, and 8-isoprostaglandin F_2α (8-isoPGF_2α).</div></div><div><h3>Results</h3><div>The median initial LPS concentration was 44.0 (37.0–57.0) pg/mL and it fell by 11.3 % at 1 month, with a further 8.3 % drop after the second month, in association with zonulin, but not with P-selectin or inflammatory markers. LPS and zonulin at baseline correlated positively with 8-isoPGF_2α. A &lt; 10 % decrease in LPS was recorded in 20 (43.5 %) patients and was more frequent in smokers, those with a complete occlusion of the infarct-related artery (IRA) and a shorter symptom duration before PCI. LPS decrease &lt;10 % was associated with a decline in IL-10 concentrations 30- and 60-days post MI. On multivariate analysis only current smoking and an initial complete IRA occlusion were independently associated with &lt;10 % decrease in LPS at 1 month (OR 10.44; 95 % CI 2.13–51.21; <em>p</em> = 0.004 and OR 6.59; 95 % CI 1.21–35.88; <em>p</em> = 0.029, respectively).</div></div><div><h3>Conclusions</h3><div>This study is the first to show factors affecting post-MI changes in LPS, highlighting the role of smoking and initial complete IRA occlusion in persistent low-grade endotoxemia following MI.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107522"},"PeriodicalIF":3.5,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144657095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Cis-regulatory elements for CRISPR-mediated transcriptional activation of the human MIR503HG locus","authors":"João P. Monteiro ,&nbsp;Francesca Vacante ,&nbsp;Azzurra L. De Pace ,&nbsp;Matthew Bennett ,&nbsp;Julie Rodor ,&nbsp;Dónal O'Carroll ,&nbsp;Joseph C. Wu ,&nbsp;Thomas Quertermous ,&nbsp;Andrew H. Baker","doi":"10.1016/j.vph.2025.107521","DOIUrl":"10.1016/j.vph.2025.107521","url":null,"abstract":"<div><div>Advances in genome annotation have revealed a striking increase in the number and complexity of non-coding RNA (ncRNA) genes, particularly multi-transcript loci that harbor long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) within the same genomic region. These loci can often function as coordinated regulatory units, with their transcription modulated by shared cis-acting regulatory elements (CREs). Traditional gene manipulation approaches, which typically target individual transcripts, are insufficient to capture the full regulatory and therapeutic potential of these complex loci. Here, we present “cis-ON” a single-vector lentiviral delivery system based on CRISPR activation (CRISPRa), designed to simultaneously upregulate multiple noncoding RNA transcripts by targeting a single CRE.</div><div>We focused on the evolutionarily conserved <em>MIR503HG</em> locus, which encodes seven lncRNA isoforms and hosts the <em>miR-424/503</em> cluster, both implicated in various cellular processes, including proliferation, angiogenesis, and endothelial-to-mesenchymal transition. Using integrative analysis of histone marks (H3K27Ac, H3K4Me3), DNase hypersensitivity, and CAGE-seq data, we identified the primary promoter of the <em>MIR503HG</em> locus. A dual fluorescent reporter screen selected optimal single guide RNAs (sgRNAs) for targeting this region. We then engineered cis-ON, a novel lentiviral system combining dCas9-VPR and sgRNA to enable a streamlined single-vector delivery approach. Transduction of primary human endothelial cells with this system robustly activated the entire locus including the <em>MIR503HG</em> isoforms and co-embedded miRNAs <em>miR-424</em> and <em>miR-503</em>, demonstrating coordinated transcriptional regulation. Additionally, the neighboring <em>LINC00629</em> lncRNA locus remained unaffected, highlighting regulatory specificity.</div><div>This approach demonstrates the feasibility of modulating complex ncRNA loci across a ∼ 10 kb genomic region by targeting a single CRE, bypassing limitations of transcriptspecific strategies. By enabling simultaneous upregulation of lncRNAs and miRNAs, the cis-ON platform provides a streamlined strategy for restoring regulatory networks disrupted in disease.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107521"},"PeriodicalIF":3.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144627290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical outcomes and safety of sotatercept in pulmonary arterial hypertension: A systematic review and meta-analysis of randomized controlled trials","authors":"Mohammad Abdulelah ,&nbsp;Chidubem Ezenna ,&nbsp;Ancy Jenil-Franco ,&nbsp;Kevin T. Jamouss ,&nbsp;Mrinal Murali Krishna ,&nbsp;Meghna Joseph ,&nbsp;Kuan-Yu Chi ,&nbsp;Talal Dahhan","doi":"10.1016/j.vph.2025.107520","DOIUrl":"10.1016/j.vph.2025.107520","url":null,"abstract":"<div><h3>Introduction</h3><div>Pulmonary arterial hypertension (PAH) remains a life-threatening condition characterized by high morbidity and mortality. However, recent therapeutic advancements have offered a paradigm shift in terms of therapeutic goals.</div></div><div><h3>Methods</h3><div>We conducted a systematic review and meta-analysis of RCTs assessing clinical outcomes and safety of sotatercept when compared to placebo in PAH. Searches of Pubmed and Cochrane Central databases were performed through April 2025. The primary outcome was all-cause mortality. Secondary outcomes included improvements in 6MWD, WHO functional class, hemodynamics, NT-proBNP, and serious adverse events. Data were pooled using a random-effects model, with certainty of evidence assessed via GRADE methodology.</div></div><div><h3>Results</h3><div>Three RCTs comprising 601 patients were included. There was a non-significant trend toward reduced mortality (RR 0.49; 95 % CI 0.16 to 1.46; <em>p</em> = 0.11). Sotatercept was associated with significant improvements in 6MWD (MD 37.99 m; 95 % CI 6.47 to 69.52; <em>p</em> = 0.04) and WHO functional class (RR 2.04; 95 % CI 1.79 to 2.31; <em>p</em> = 0.002). Hemodynamic improvements included reductions in PVR (MD -237.73 dyn·s/cm⁵; 95 % CI -367.02 to −1.8.43; <em>p</em> = 0.02) and mPAP (MD -14.88 mmHg; 95 % CI -24.76 to −4.99; p = 0.02). Serious adverse events were similar (RR 0.79; 95 % CI 0.51 to 1.23; <em>p</em> = 0.15).</div></div><div><h3>Conclusion</h3><div>Sotatercept significantly improves functional and hemodynamic outcomes in PAH, with a favorable safety profile. While mortality benefits remain uncertain, these findings support its clinical utility as an emerging therapy in PAH.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107520"},"PeriodicalIF":3.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of histone modifications in pulmonary hypertension: From mechanisms to therapeutic targets","authors":"Yunhua Yang ,&nbsp;Shaoxin Gong ,&nbsp;Na Liang ,&nbsp;Zhouxin Li ,&nbsp;Xiaoyu Duan ,&nbsp;Tong Xie ,&nbsp;Xiaoyong Lei ,&nbsp;Aiping Wang","doi":"10.1016/j.vph.2025.107519","DOIUrl":"10.1016/j.vph.2025.107519","url":null,"abstract":"<div><div>Pulmonary hypertension is a progressive vascular disease characterized by pulmonary vascular remodeling, with high mortality and poor prognosis despite advances in medical therapy. Recently, histone modification therapies for pulmonary hypertension have received more attention. Studies have shown that abnormal histone modifications and the enzymes responsible for these alterations can drive pulmonary vascular cell proliferation, migration, and anti-apoptosis by regulating chromatin structure and gene expression, thereby promoting pulmonary vascular remodeling in pulmonary hypertension. This review illustrates histone modifications, including methylation, acetylation, lactylation, and SUMOylation, and the enzymes responsible for these modifications, exploring their role and pathophysiological mechanism in pulmonary hypertension. In addition, the review summarizes the small molecule modulators currently under development and their efficacy in various preclinical models of pulmonary hypertension. Comprehending the function of histone modifications in pulmonary hypertension will help identify new biomarkers and molecular targets and facilitate personalized treatments for this severe disease.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107519"},"PeriodicalIF":3.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of simvastatin treatment on leptomeningeal collateral vessels: resistance, number and diameter","authors":"Fern Williams ,&nbsp;Kristy Martin ,&nbsp;Thomas R. Scott ,&nbsp;David Clark ,&nbsp;Merce Fuentes Amell ,&nbsp;Neil J. Spratt ,&nbsp;Daniel J. Beard ,&nbsp;Kirsten G. Coupland","doi":"10.1016/j.vph.2025.107518","DOIUrl":"10.1016/j.vph.2025.107518","url":null,"abstract":"<div><div>Good leptomeningeal collateral vessels (LMC) are associated with smaller lesion volume and better patient outcomes from ischaemic stroke, but their architecture varies greatly between individuals. Statins can stimulate angiogenesis and show promise for stimulating cerebral collaterogenesis. Statins could thus improve LMC grade and ensure all patients receive positive outcomes from treatment. This potentially explains why statin treatment is effective given prior to stroke in pre-clinical models, but not prescribed afterwards in clinical trials.</div><div>LMC-rich C57Bl/6 and LMC-poor BALB/c 12-week-old male mice were randomised to receive daily oral simvastatin (10 mg/kg) or vehicle for 4 weeks. The cerebrovasculature was silicone-perfused, allowing LMC numbers and dimensions to be analysed. Values for tortuosity, vascularity and LMC resistance were calculated.</div><div>In BALB/c, estimated resistance was lower with simvastatin treatment (vehicle: 0.104 ± 0.09, simvastatin: 0.023 ± 0.02; <em>p</em> = 0.04) and LMC numbers were greater (vehicle: 1.6 ± 1.6, simvastatin: 4.0 ± 3.2; <em>p</em> = 0.04). In C57Bl/6, there was no difference to resistance, but LMCs were smaller in diameter (vehicle: 16.3 ± 1.8 μm, simvastatin: 14.0 ± 1.4 μm, <em>p</em> = 0.008). Statin-treated C57Bl/6 also had more arterial branchpoints (left hemisphere, vehicle: 363.8 ± 55 per cm2, simvastatin: 417.3 ± 58 per cm2, <em>p</em> = 0.007; right, vehicle: 315.1 ± 40 per cm2, simvastatin: 397.5 ± 43 per cm2, <em>p</em> &lt; 0.0001).</div><div>We have observed signs of collaterogenesis and angiogenesis, providing evidence that statins stimulate growth of LMCs. Greatest benefit was seen in LMC-poor BALB/c, suggesting that patients with poor LMC circulation stand to gain most from LMC-enhancing therapies. Patients receiving statins prior to stroke have likely developed better LMCs, leading to better stroke outcomes. These findings should stimulate investigation of further safe, widely-available LMC-enhancing therapies.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107518"},"PeriodicalIF":3.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Explosive discovery, surprising future: The extraordinary journey of nitroglycerin, nitroderivatives and nitric oxide","authors":"Maria Rosa Montinari ,&nbsp;Sergio Minelli ,&nbsp;John D. Horowitz ,&nbsp;Raffaele De Caterina","doi":"10.1016/j.vph.2025.107517","DOIUrl":"10.1016/j.vph.2025.107517","url":null,"abstract":"<div><div>For over 150 years, nitrates have been a cornerstone in the treatment of cardiovascular disease. Nitroglycerin — synthesized by Italian chemist Ascanio Sobrero in 1847 — was initially used in explosives, as the main component of dynamite, by Alfred Nobel. The Scottish physician Lauder Brunton first used amyl nitrite for angina in 1867, and in 1879 the English physician William Murrell described the benefits of nitroglycerin for angina pectoris. Organic nitrates, including nitroglycerin, act as nitric oxide donors, sharing the mechanism of NO release, which induces vasodilation. This paper reviews the fascinating history of nitroglycerin and nitroderivatives, the related discovery of nitric oxide as a cardiovascular signaling molecule, and the 1998 Nobel Prize awarded for this discovery. The paper also succinctly explores current and future roles of nitric oxide donors in cardiovascular treatment.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"160 ","pages":"Article 107517"},"PeriodicalIF":3.5,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144470863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}