Journal of Cardiovascular Translational Research最新文献_第2页

Glutaminase 1 in Vascular Disease: Linking Metabolic Reprogramming to Atherosclerosis Progression and Stability. 谷氨酰胺酶1在血管疾病中的作用：将代谢重编程与动脉粥样硬化的进展和稳定性联系起来。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-11 DOI: 10.1007/s12265-026-10743-1

Xi-Long Zheng, Hao Yin, Zhihan Tang, Zhixin Shan, Xiaoyan Dai

{"title":"Glutaminase 1 in Vascular Disease: Linking Metabolic Reprogramming to Atherosclerosis Progression and Stability.","authors":"Xi-Long Zheng, Hao Yin, Zhihan Tang, Zhixin Shan, Xiaoyan Dai","doi":"10.1007/s12265-026-10743-1","DOIUrl":"https://doi.org/10.1007/s12265-026-10743-1","url":null,"abstract":"Glutaminase-1 (GLS1) converts glutamine to glutamate, fueling anaplerosis, redox defense, and biosynthesis. We synthesize animal, cellular, and human (bulk/single-cell) data to define cell- and stage-specific roles of GLS1 in atherosclerosis and to outline translational opportunities. In early disease, GLS1 drives vascular smooth muscle proliferation, endothelial sprouting, and inflammatory macrophage activation, promoting plaque growth and neovascularization. In advanced plaques, GLS1 sustains fibrous-cap VSMC survival, endothelial barrier function, and macrophage efferocytosis, limiting necrosis and enhancing stability; excessive glutamate may favor calcification. We also connect GLS1 to vascular senescence and ferroptosis. We propose precision use of GLS1 modulation: a proof-of-concept strategy is short-term telaglenastat (CB-839) after angioplasty to curb neointimal hyperplasia, guided by glutamine-PET and biomarkers to avoid destabilizing mature plaques. GLS1 emerges as a tunable metabolic checkpoint whose effects depend on cell state and disease stage; judicious, time-limited modulation could complement lipid-lowering and anti-inflammatory therapies in cardiovascular disease.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433063","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}

引用次数: 0

Past, Present and Future of Regenerative Gene Therapy for Ischemic Heart Failure. 再生基因治疗缺血性心力衰竭的过去、现在和未来。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-11 DOI: 10.1007/s12265-025-10731-x

Laura Florit Gonzalez, Mara Bouwman, Jeroen Bakkers

引用次数: 0

Comprehensive Analysis of Bulk RNA-seq, Machine Learning, Mendelian Randomization, and Single-Cell Sequencing Unravels SLC22A3 as a Solute Carrier Superfamily-Associated Biomarker in Atherosclerosis. 大量rna测序、机器学习、孟德尔随机化和单细胞测序的综合分析揭示了SLC22A3是动脉粥样硬化中溶质载体超家族相关的生物标志物。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-10 DOI: 10.1007/s12265-026-10757-9

Yongchao Yu, Lan Wang, Tianhui Wang, Ya Zhang, Xiaomeng Su, Xingyang Dai, Xiangang Mo

{"title":"Comprehensive Analysis of Bulk RNA-seq, Machine Learning, Mendelian Randomization, and Single-Cell Sequencing Unravels SLC22A3 as a Solute Carrier Superfamily-Associated Biomarker in Atherosclerosis.","authors":"Yongchao Yu, Lan Wang, Tianhui Wang, Ya Zhang, Xiaomeng Su, Xingyang Dai, Xiangang Mo","doi":"10.1007/s12265-026-10757-9","DOIUrl":"https://doi.org/10.1007/s12265-026-10757-9","url":null,"abstract":"Growing evidence implicates solute carrier (SLC) superfamily in atherosclerosis (AS) pathogenesis. This study identified SLC22A3 as a novel AS biomarker and therapeutic target using multi-omics analysis. Integrating WGCNA and machine learning (LASSO, SVM-RFE, XGBoost, Random Forest) on bulk RNA-seq (GSE43292) pinpointed SLC22A3. External datasets (GSE28829, GSE163154) confirmed significant SLC22A3 downregulation in AS (P < 0.001) and high diagnostic accuracy (AUC > 0.9). SMR analysis revealed a causal genetic link between SLC22A3 expression and reduced AS risk (P < 0.05, OR = 0.512 (95% CI: 0.280-0.939))). scRNA-seq showed SLC22A3 specifically expressed in smooth muscle cells (SMCs), significantly reduced in symptomatic patients. Molecular docking and molecular dynamics simulation nominated six FDA-approved drugs as potential SLC22A3-targeting therapeutics. Experimental validation further confirmed the significant downregulation of SLC22A3 at both mRNA and protein levels. SLC22A3 is a promising diagnostic biomarker and therapeutic target for AS, functionally linked to SMCs.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433051","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}

引用次数: 0

Impact of E-Cigarette Use on Circadian Proteins and Cardiovascular Risk Markers. 电子烟使用对昼夜蛋白和心血管风险标志物的影响。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-09 DOI: 10.1007/s12265-026-10762-y

Ayman Alzu'bi, Ejlal Abu-El-Rub, Ramada R Khaswaneh, Mohammed Al-Zubaidi, Wissam Almomani, Abdelrahman Alenaizat, Adnan H Ayyash, Anas Alragheb, Anas Alshannag, Enas Ahmad, Mai Elaarag, Raed M Al-Zoubi

{"title":"Impact of E-Cigarette Use on Circadian Proteins and Cardiovascular Risk Markers.","authors":"Ayman Alzu'bi, Ejlal Abu-El-Rub, Ramada R Khaswaneh, Mohammed Al-Zubaidi, Wissam Almomani, Abdelrahman Alenaizat, Adnan H Ayyash, Anas Alragheb, Anas Alshannag, Enas Ahmad, Mai Elaarag, Raed M Al-Zoubi","doi":"10.1007/s12265-026-10762-y","DOIUrl":"10.1007/s12265-026-10762-y","url":null,"abstract":"The increasing popularity of E-cigarettes among young adults has raised concerns about their health effects, particularly on the circadian system, which regulates critical physiological processes. This study examined how vaping influences circadian proteins and inflammatory markers, comparing these effects to those in cardiovascular disease patients. Blood samples from 254 participants, non-vaping controls (n = 90), regular vapers (n = 86), and cardiovascular patients (n = 78), were analyzed for circadian proteins (Melatonin, BMAL1, PER1, PER2, CRY1, CRY2) and inflammatory/oxidative stress markers (IFN-γ, MDA). Vaping significantly decreased Melatonin, PER1, PER2, CRY1, and CRY2, while BMAL1 remained unchanged. Elevated IFN-γ and MDA levels indicated increased inflammation and oxidative stress in vapers. Vaping induces circadian disruption patterns similar to cardiovascular disease, suggesting a potential mechanism linking e-cigarette use to increased cardiovascular risk.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biorefine, a Transcatheter Mitral Annulus Ablation System for the Treatment of Mitral Regurgitation: Pre-Clinical Study in Sheep. 经导管二尖瓣环消融系统治疗二尖瓣反流：绵羊临床前研究。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-09 DOI: 10.1007/s12265-026-10763-x

Avi Avner, Leor Perl

引用次数: 0

Endothelial Dysfunction: Insights into Systemic Lupus Erythematosus-associated Cardiovascular Disease and Neuropsychiatric Manifestations. 内皮功能障碍：系统性红斑狼疮相关心血管疾病和神经精神表现的见解。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-07 DOI: 10.1007/s12265-026-10753-z

Helen M Butler, Marie Elaine Zehntner, Justin P Van Beusecum

引用次数: 0

Mitochondrial Resilience: Unraveling the Triadic Interplay of Phosphocreatine, Cyclophilin D, and STAT3 in Heart Failure. 线粒体恢复力：揭示磷酸肌酸、亲环蛋白D和STAT3在心力衰竭中的三重相互作用。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-06 DOI: 10.1007/s12265-026-10756-w

Eskandar Qaed, Wu Liu, Waleed Aldahmash, Mueataz A Mahyoub, Haya A Elshafei, Zeyao Tang

{"title":"Mitochondrial Resilience: Unraveling the Triadic Interplay of Phosphocreatine, Cyclophilin D, and STAT3 in Heart Failure.","authors":"Eskandar Qaed, Wu Liu, Waleed Aldahmash, Mueataz A Mahyoub, Haya A Elshafei, Zeyao Tang","doi":"10.1007/s12265-026-10756-w","DOIUrl":"10.1007/s12265-026-10756-w","url":null,"abstract":"Heart failure remains a major global health burden, with mitochondrial dysfunction recognized as a key contributor to its onset and progression. This review highlights three critical regulators of mitochondrial integrity phosphocreatine (PCr), cyclophilin D (CypD), and signal transducer and activator of transcription 3 (STAT3) and their coordinated roles in cardiac function. PCr is vital for sustaining myocardial energy balance, particularly under metabolic stress. CypD controls the mitochondrial permeability transition pore, regulating cell death pathways that contribute to cardiac injury. Beyond its classical nuclear actions, STAT3 supports mitochondrial respiration, biogenesis, and resistance to oxidative damage. Evidence reveals a functional interplay among these regulators, forming a protective network that preserves mitochondrial performance. Disruption of this network promotes energetic failure, mitochondrial injury, and heart failure progression. Targeting PCr metabolism, CypD activity, and STAT3 signaling may represent a promising therapeutic approach to enhance mitochondrial resilience and improve clinical outcomes in heart failure patients.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365399","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}

引用次数: 0

Artificial Intelligence and Machine Learning Applications in Fibromuscular Dysplasia: Transforming Diagnosis, Risk Stratification, and Clinical Decision-Making. 人工智能和机器学习在纤维肌肉发育不良中的应用：转化诊断、风险分层和临床决策。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-06 DOI: 10.1007/s12265-026-10760-0

Ali Hamza, Muneeb Faiz, Aliha Iftikhar, Bakhtawar Badal, Sakeena Qamar, Eisha Ali, Muhammad Usman, Muhammad Talha, Noor Un Nisa, Amna Mujtaba, Awais Butt, Noor Fatima Talat, Ayesha Ashraf

{"title":"Artificial Intelligence and Machine Learning Applications in Fibromuscular Dysplasia: Transforming Diagnosis, Risk Stratification, and Clinical Decision-Making.","authors":"Ali Hamza, Muneeb Faiz, Aliha Iftikhar, Bakhtawar Badal, Sakeena Qamar, Eisha Ali, Muhammad Usman, Muhammad Talha, Noor Un Nisa, Amna Mujtaba, Awais Butt, Noor Fatima Talat, Ayesha Ashraf","doi":"10.1007/s12265-026-10760-0","DOIUrl":"10.1007/s12265-026-10760-0","url":null,"abstract":"Fibromuscular dysplasia (FMD) is a non-atherosclerotic vascular disorder with heterogeneous presentations, making diagnosis and management highly dependent on imaging and clinical expertise. This narrative review examines how artificial intelligence (AI) and machine learning (ML) are transforming FMD care. AI-enhanced imaging, particularly convolutional neural network-based analysis, improves detection of the characteristic \"string-of-beads\" pattern on CT angiography, magnetic resonance angiography, and ultrasound, although FMD-specific validation remains limited. ML models facilitate risk stratification, prediction of disease progression, and early identification of complications such as aneurysms and stroke by integrating clinical, imaging, and genomic data. AI-driven clinical decision support systems further enable personalized treatment selection through pharmacogenomic insights and robot-assisted interventions. Despite promising real-world applications, challenges persist, including limited large-scale datasets, workflow integration, regulatory barriers, and algorithmic bias affecting underrepresented populations. Future advances in explainable AI, federated learning, and digital health integration may enable a shift toward predictive, patient-centered FMD management.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365433","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}

引用次数: 0

Silent Myocardial Infarction Revisited: Immuno-metabolic Mechanisms, Multimodal Biomarkers, and Translational Diagnostics. 重新审视无症状心肌梗死：免疫代谢机制、多模式生物标志物和转化诊断。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-05 DOI: 10.1007/s12265-026-10755-x

Yashvi Pethani, Neha Pethani, Dilip Pethani, Rima Shah, Darshil Shah, Jignesh Shah

{"title":"Silent Myocardial Infarction Revisited: Immuno-metabolic Mechanisms, Multimodal Biomarkers, and Translational Diagnostics.","authors":"Yashvi Pethani, Neha Pethani, Dilip Pethani, Rima Shah, Darshil Shah, Jignesh Shah","doi":"10.1007/s12265-026-10755-x","DOIUrl":"10.1007/s12265-026-10755-x","url":null,"abstract":"Silent Myocardial Infarction (SMI) is a clinically underrecognized phenotype along the myocardial infarction continuum that progresses without anginal symptoms. Its prevalence in diabetes, chronic kidney disease, and the elderly reflects contributions from neuropathy, autonomic dysfunction, and neurogenic silencing. Emerging evidence indicates that SMI reflects a biologically biased phenotype within the myocardial infarction continuum shaped by immune-metabolic and neurogenic modulation rather than representing a distinct entity. Biomarkers such as sCD36, galectin-3, sST2, and GDF-15 capture fibrotic and inflammatory remodeling, while NETosis-linked markers (CitH3, MPO-DNA) highlight thrombo-inflammation. Lipidomic stressors, including ceramides and β-hydroxybutyrate, further define ischemic burden. Spatial omics and single-cell analyses identify enrichment of immune-regulatory macrophage programs associated with restrained inflammation without establishing the causality for symptom absence. A tiered approach-biomarker screening followed by imaging-supports risk stratification. This review integrates mechanistic and translational insights, proposing a pragmatic framework for early diagnosis and biologically aligned treatment of SMI.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355330","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}

引用次数: 0

Takotsubo Syndrome: The First Non-Acute Proteomic Analysis by Remote Dried Blood Microsampling. Takotsubo综合征：第一个非急性蛋白质组学分析通过远程干血显微取样。

IF 2.5 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-02-27 DOI: 10.1007/s12265-026-10752-0

Paul Marano, Kirstin Washington, Blandine Chazarin, Niveda Sundararaman, Koen Raedschelders, Jenna Maughan, Okezi Obrutu, Benita Tjoe, Romana Herscovici, Prizzi Moy, Chrisandra Shufelt, Thomas Rutledge, Alexander Polyak, Sandy Joung, Yunxian Liu, Susan Cheng, Janet Wei, Jennifer E Van Eyk, C Noel Bairey Merz

{"title":"Takotsubo Syndrome: The First Non-Acute Proteomic Analysis by Remote Dried Blood Microsampling.","authors":"Paul Marano, Kirstin Washington, Blandine Chazarin, Niveda Sundararaman, Koen Raedschelders, Jenna Maughan, Okezi Obrutu, Benita Tjoe, Romana Herscovici, Prizzi Moy, Chrisandra Shufelt, Thomas Rutledge, Alexander Polyak, Sandy Joung, Yunxian Liu, Susan Cheng, Janet Wei, Jennifer E Van Eyk, C Noel Bairey Merz","doi":"10.1007/s12265-026-10752-0","DOIUrl":"10.1007/s12265-026-10752-0","url":null,"abstract":"Takotsubo syndrome (TTS) is an under-recognized form of acute-onset heart failure typically precipitated by stress. While recovery of cardiac function is described over the course of weeks, adverse outcomes after apparent recovery are increasingly recognized. However, the pathophysiology of non-acute manifestations remains poorly understood. We used mass-spectrometry-based discovery proteomics from remotely collected non-acute dried blood microsamples to perform a case-control study in 62 participants with a prior TTS episode (median of 2.24 years prior to sample collection) and 47 reference controls. We quantified 398 unique proteins, and found that agnostic clustering techniques showed separation between TTS and reference control samples. This represents the first proteomic characterization of non-acute TTS. Pathway analysis of the 52 differentially regulated proteins demonstrated enrichment of proteins involved in complement activation, nitric oxide signaling, and with antioxidant activity. These enriched pathways may be suggestive of a persistent cardiomyopathy resulting from or predisposing to TTS.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12948850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147317033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0