Arteriosclerosis, Thrombosis, and Vascular Biology最新文献

{"title":"miR-146a Deficiency Ablates β-Aminopropionitrile-Induced Thoracic Aortic Aneurysmal Rupture in Mice.","authors":"Nithya Ramesh, Edward Downey, Sudheer Kumar Kanumuri, Laiba Anwar, Zhenguo Liu, Venkateswaran Subramanian","doi":"10.1161/ATVBAHA.126.324360","DOIUrl":"10.1161/ATVBAHA.126.324360","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e324360"},"PeriodicalIF":8.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148270065","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":"Brushing Your Teeth May Save Your Aorta: <i>Fusobacterium nucleatum-</i>Derived Isoleucine Drives Aneurysm Progression Through Epigenetic Reprogramming of Vascular Smooth Muscle Cells.","authors":"Lanting Hu, Zhenjie Liu","doi":"10.1161/ATVBAHA.126.325065","DOIUrl":"10.1161/ATVBAHA.126.325065","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e325065"},"PeriodicalIF":8.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148270049","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":"Financial Toxicity: Inequities and Impact on Cardiovascular Disease.","authors":"Clarke Morihara, Kevin Benavente, Charlotte Park, Hafeez Ul Hassan Virk, Dina Abushanab, Laurence S Sperling, Yochai Birnbaum, Salim S Virani, Carl J Lavie, Chayakrit Krittanawong","doi":"10.1161/ATVBAHA.125.324015","DOIUrl":"10.1161/ATVBAHA.125.324015","url":null,"abstract":"<p><p>Healthcare costs are ever increasing, with impacts across all socioeconomic backgrounds. As a result, financial strain and financial toxicity are a consequences of rising healthcare costs and economic variations, with significant negative impacts on cardiovascular disease. This review explores financial toxicity and the interplay of net worth, financial mobility, and social determinants of health in cardiovascular disease while also addressing the role of advocacy and policy in public health. Given the significant multidimensional aspects of financial toxicity, understanding its impact on cardiovascular disease is crucial to improving outcomes on a population-wide scale.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e324015"},"PeriodicalIF":8.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148315338","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":"Enabling Technologies in Vascular Biology: Microphysiological Systems, Organoids, and Beyond.","authors":"Hanieh Gholizadeh, Kambez H Benam","doi":"10.1161/ATVBAHA.126.323054","DOIUrl":"10.1161/ATVBAHA.126.323054","url":null,"abstract":"<p><p>Vascular and cardiovascular diseases are leading causes of mortality globally. Despite significant progress in elucidating the molecular and cellular mechanisms involved in these conditions, some critical aspects, including complex intercellular interactions and therapeutic efficacy, require further investigation to be fully understood and predicted. This lack of knowledge motivates the development of advanced research methodologies, where bioengineering has contributed significantly. Technological advances in bioengineering have evolved into powerful tools that replicate the molecular and cellular microenvironment of human vascular and cardiac tissues with unprecedented fidelity in vitro and ex vivo. The evolution of conventional 2-dimensional, monocultured cell models into 3-dimensional and mechanically dynamic models that also possess tissue-level cellular and molecular sophistications enables studying vascular pathologies and therapies with promising predictability. Various techniques, such as microphysiological systems, organoids, and bioprinting, are increasingly used and further improved through numerous studies to reconstruct human vascular microenvironment and the associated diseases such as atherosclerosis and thrombosis in vitro. Despite these advancements, there are still challenges with each of these methods in addition to the knowledge gaps left for future research. This review takes a critical approach to comprehensively review existing reports and the most recent progress in the application of cutting-edge in vitro and ex vivo technologies for vascular biology and pathology. More importantly, it highlights the challenges and research gaps that will require future research to be addressed.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e323054"},"PeriodicalIF":8.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366854","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":"Cardiovascular Risk Reduction: What Can Brown (Adipose Tissue) Do for You?","authors":"Khanh-Van Tran, Timothy P Fitzgibbons","doi":"10.1161/ATVBAHA.126.324981","DOIUrl":"10.1161/ATVBAHA.126.324981","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e324981"},"PeriodicalIF":8.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155139","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":"Mitochondrial Extracellular Vesicles Enhance Aortic Valve Calcification Via Carnitine O-Octanoyltransferase-Brief Report.","authors":"Rei Itagawa, Takehito Okui, Takeshi Tanaka, Yuto Nakamura, Daiki Hosokawa, Cassandra L Clift, Mark C Blaser, Taku Kasai, Luisa Weiss, Mandy E Turner, Marie Billaud, Masanori Aikawa, Sasha A Singh, Elena Aikawa","doi":"10.1161/ATVBAHA.126.324456","DOIUrl":"10.1161/ATVBAHA.126.324456","url":null,"abstract":"<p><strong>Background: </strong>Calcific aortic valve disease, commonly manifesting as aortic stenosis, is a leading cause of mortality with no effective therapy. We previously identified CROT (carnitine O-octanoyltransferase) as a mediator of mitochondrial dysfunction and vascular calcification; however, its role in calcific aortic valve disease is unknown. We investigated whether CROT promotes calcific aortic valve disease progression through the release of procalcific mitochondria-derived extracellular vesicles (mitoEVs).</p><p><strong>Methods: </strong>Human valvular interstitial cells were isolated from aortic valves of patients with aortic stenosis (n=49; n=34 males, n=15 females). Calcification was induced with osteogenic medium and assessed by Alizarin red. Proteomics compared valvular interstitial cells cultured in normal medium or osteogenic medium following scramble or <i>CROT</i> siRNA to define CROT-dependent pathways. Mitochondrial function was evaluated by Seahorse XF analysis (oxygen consumption rate) and morphology by MitoTracker staining. Extracellular vesicles were isolated by ultracentrifugation and characterized using NanoSight Pro. In vivo, aortic stenosis was induced by aortic valve wire injury in <i>Ldlr</i>^<i>-/-</i><i>Crot</i>^<i>+/+</i> (Sham, n=12; aortic valve wire injury, n=19) and <i>Ldlr</i>^<i>-</i>^<i>/-</i><i>Crot</i>^<i>-</i>^<i>/-</i> (aortic valve wire injury, n=23) mice. Disease progression was monitored by echocardiography, and calcification was visualized using OsteoSense680EX imaging.</p><p><strong>Results: </strong>CROT silencing significantly reduced osteogenic medium-induced calcification in valvular interstitial cells (<i>P</i><0.05). Proteomics revealed alterations in mitochondria-associated proteins following siCROT. Osteogenic medium-induced mitochondrial fragmentation and increased mitoEV release were attenuated by CROT silencing. Immunofluorescence revealed mitoEVs localized to calcified extracellular regions. In vivo, CROT deficiency reduced valvular calcification and attenuated aortic stenosis progression.</p><p><strong>Conclusions: </strong>Osteogenic stress drives mitochondrial fragmentation and procalcific mitoEV release. CROT inhibition restores mitochondrial homeostasis, reduces mitoEV release and calcification, identifying CROT as a potential therapeutic strategy for calcific aortic valve disease.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e324456"},"PeriodicalIF":8.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13155380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833103","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":"Thrombus and Aortic Wall ¹⁸F-FDG Positron Emission Tomography Uptake in Abdominal Aortic Aneurysms.","authors":"Mireia Bragulat-Arévalo, Andrea Guala, Marta Ferrer-Cornet, Marvin García-Reyes, Juan Garrido-Oliver, Ruper Oliveró-Soldevila, Alba Catala-Santarrufina, Pere Lopez-Gutierrez, Ignacio Ferreira-González, Jose Rodríguez-Palomares, Sergi Bellmunt-Montoya, Lydia Dux-Santoy","doi":"10.1161/ATVBAHA.126.324343","DOIUrl":"10.1161/ATVBAHA.126.324343","url":null,"abstract":"<p><strong>Background: </strong>Most abdominal aortic aneurysms (AAA) present intraluminal thrombus (ILT). Whether its role is detrimental or protective for AAA evolution and patients outcomes is debated. ¹⁸F-fluorodeoxyglucose positron emission tomography analysis in patients with AAA has shown contradictory results and has not widely explored ILT. The aim of this cross-sectional study was to investigate the colocalized association between ¹⁸F-fluorodeoxyglucose and ILT presence and characteristics in AAA.</p><p><strong>Methods: </strong>Consecutive patients with infrarenal AAA were prospectively enrolled and underwent positron emission tomography/magnetic resonance imaging. From the abdominal aorta segmentation, an aortic wall volume was defined and discretized into 28 standardized aortic patches, permitting colocalized interpatient and intrapatient analyses. The target-to-background ratio (TBR) was extracted in each patch, and extremely low (coldspots) and high (hotspots) absorption areas were computed. Local AAA diameters and ILT characteristics were computed in each patch. Linear mixed-effect models were used to test the association between AAA and ILT characteristics and ¹⁸F-fluorodeoxyglucose uptake.</p><p><strong>Results: </strong>Thirty-six patients (median age, 73 [interquartile range, 68-77] years, 31 [86.1%] men) completed the protocol. The AAA maximum diameter was 49.6 (45.0-56.2) mm, and most patients (28 [77.8%]) presented ILT. Patients with thrombus presented higher coldspot area and lower hotspot area (<i>P</i><0.001). Patches in nondilated regions presented higher TBR compared with AAA patches (<i>P</i><0.001), which showed a negative association of TBR with local diameter (<i>β</i>=-0.006) and thrombus presence (<i>β</i>=-0.003). TBR decreased with increased ILT coverage (<i>β</i>=-0.002), while coldspot area increased (<i>β</i>=0.046). In both the ILT and thrombus-covered wall, TBR decreased with increasing ILT thickness.</p><p><strong>Conclusions: </strong>Decreased metabolic activity as per 18-fluorodeoxyglucose positron emission tomography is observed in the AAA wall compared with the nondilated abdominal region. This effect is exacerbated by local thrombus presence and thickness, suggesting that ILT contributes to the further degradation of the aortic wall in the diseased region.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e324343"},"PeriodicalIF":8.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833051","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":"<i>S</i>-Adenosylhomocysteine Hydrolase (SAHH) at the Crossroads of Metabolism, Epigenetics, and Plaque Stability.","authors":"Ravi K Komaravolu","doi":"10.1161/ATVBAHA.126.325025","DOIUrl":"https://doi.org/10.1161/ATVBAHA.126.325025","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":"46 7","pages":"e325025"},"PeriodicalIF":8.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148315457","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 II Induces Abdominal Aortic Branch Aneurysms in <i>Fibrillin-1</i> ^{<i>C1041G/+</i>} Mice-Brief Report.","authors":"Michael K Franklin, Deborah A Howatt, Jessica J Moorleghen, Mary B Sheppard, Yuriko Katsumata, Hisashi Sawada, Hong S Lu, Alan Daugherty","doi":"10.1161/ATVBAHA.125.324124","DOIUrl":"10.1161/ATVBAHA.125.324124","url":null,"abstract":"<p><strong>Background: </strong>Mice harboring a missense variant (C1041G) of <i>Fbn1</i> have been used extensively for aortopathy research, but do not mimic all facets of the human disease. The role of increased AngII (angiotensin II) or blood pressure in determining the arterial phenotype of these mice remains incompletely defined. The purpose of this study was to determine whether AngII, either directly or indirectly through increased blood pressure, promotes pathology in the proximal thoracic aorta and beyond.</p><p><strong>Methods: </strong><i>Fbn1</i>^<i>+/+</i> <i>and Fbn1</i>^C1041G/+ littermates were infused with either AngII or norepinephrine via subcutaneously implanted osmotic pumps. Microcomputed tomography was used to visualize vascular pathologies. Maximal arterial dimensions were measured using in situ or microcomputed tomography images.</p><p><strong>Results: </strong>AngII infusion dramatically augmented aortopathy in <i>Fbn1</i>^C1041G/+ mice. Aortic dissection was visible within 3 days of AngII infusion. Over 50% of male <i>Fbn1</i>^C1041G/+ mice died during AngII infusion, primarily due to aortic rupture in either the thoracic or abdominal regions. Surviving males had increased ascending and suprarenal aortic diameters and developed pathological lesions at the celiac and superior mesenteric branches of the abdominal aorta. Female mice had a much lower incidence of death but had increased ascending aortic and branch diameters. Although norepinephrine infusion also increased systolic blood pressure, it did not affect mortality or enlarge aortic or branch diameters in <i>Fbn1</i>^C1041G/+ mice. While microcomputed tomography identified novel pathological changes during AngII infusion, including the development of aortic branch aneurysms in the celiac and superior mesenteric arteries, the maximal diameters of the adjacent suprarenal aorta showed only modest increases in male <i>Fbn1</i>^C1041G/+ mice.</p><p><strong>Conclusions: </strong>AngII exacerbated aortic pathology in <i>Fbn1</i>^C1041G/+ mice. It also promoted the development of pathologies at aortic branch points, including the celiac and superior mesenteric arteries.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e324124"},"PeriodicalIF":8.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13220914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148040575","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":"Abdominal Fat Measures Are Associated With Sex-Specific Prothrombotic Changes in Middle-Aged Adults.","authors":"Judith P L Verlaan, Luuk J J Scheres, Frits R Rosendaal, Victor E A Gerdes, Hildo J Lamb, Vânia M Morelli, Ton Lisman, Renée de Mutsert, Suzanne C Cannegieter, Astrid van Hylckama Vlieg","doi":"10.1161/ATVBAHA.125.324252","DOIUrl":"10.1161/ATVBAHA.125.324252","url":null,"abstract":"<p><strong>Background: </strong>A high body mass index is an important risk factor for venous thromboembolism. However, high body mass index does not necessarily reflect an unhealthy body fat distribution. Therefore, we evaluated the association between the amount of visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue, and liver fat content with venous thromboembolism-associated coagulation parameters: plasma levels of factor (F) VIII, FIX, FXI, fibrinogen, and thrombin generation (endogenous thrombin potential and peak thrombin).</p><p><strong>Methods: </strong>In 1759 participants of the NEO study (the Netherlands Epidemiology of Obesity), VAT and abdominal subcutaneous adipose tissue were assessed with magnetic resonance imaging, and liver fat with ¹H-MR spectroscopy. Through linear regression, we examined cross-sectional associations between quartiles of body fat measures and coagulation parameters, stratified by sex and adjusted for relevant confounders.</p><p><strong>Results: </strong>We found that the amount of VAT was associated with all coagulation parameters in a dose-response manner, with higher levels for individuals in quartile 4 versus 1, ranging between 5.2% (95% CI, -5.8 to 17.4) for FVIII in men and 21.0% (95% CI, 16.7-25.5) for FIX in women. In women, the amount of abdominal subcutaneous adipose tissue was associated with all coagulation parameters, with the highest percentual difference between quartile 4 versus 1 for endogenous thrombin potential 25.4% (95% CI, 13.7-38.4). Liver fat was mostly associated with higher FIX in both sexes, 13.2% (95% CI, 8.6-18.0) in men and 13.6% (95% CI, 10.0-17.4) in women.</p><p><strong>Conclusions: </strong>The strongest prothrombotic associations were found for VAT. Abdominal subcutaneous adipose tissue contributed only in women, though less strongly than VAT, indicating sex-specific associations. Liver fat was consistently associated with FIX. These findings underscore the importance of body fat distribution and sex in coagulation and thrombotic potential.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e324252"},"PeriodicalIF":8.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147926034","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}