Journal of Cardiovascular Translational Research最新文献_第10页

Traditional Chinese Medicine Targeting Ferroptosis in Cardiovascular Diseases: Advances and Perspectives. 中医药治疗心血管疾病铁下垂的研究进展与展望

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-04-15 DOI: 10.1007/s12265-026-10769-5

Jianing Wang, Yuetong Li, Yuan Liu, Zihui Zhang, Heng Ma

引用次数: 0

Mechanistic Insights into Therapeutic Strategies for Post- Menopausal Atherosclerosis: Evidence from an Ovariectomized Mouse Model. 绝经后动脉粥样硬化治疗策略的机制见解：来自卵巢切除小鼠模型的证据。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-30 DOI: 10.1007/s12265-026-10766-8

Siti Bazilah Zulkefli, Fathimah Mohamad, Nurul Alimah Abdul Nasir, Ahmad Nazrun Shuid, Nasibah Azme

{"title":"Mechanistic Insights into Therapeutic Strategies for Post- Menopausal Atherosclerosis: Evidence from an Ovariectomized Mouse Model.","authors":"Siti Bazilah Zulkefli, Fathimah Mohamad, Nurul Alimah Abdul Nasir, Ahmad Nazrun Shuid, Nasibah Azme","doi":"10.1007/s12265-026-10766-8","DOIUrl":"10.1007/s12265-026-10766-8","url":null,"abstract":"Atherosclerosis in postmenopausal women is a significant cardiovascular complication that is caused by estrogen deficiency, leading to increased inflammation and oxidative stress, and dysregulated lipid metabolism. The review summarizes the evidence gathered in ovariectomized mice models in order to determine mechanistic associations between different pharmacological therapeutic strategies and their impact on the progression of atherosclerosis in postmenopausal conditions. This review builds on an upstream hormonal signaling framework model of estrogen receptor-mediated pathways and the three main downstream mechanistic pillars: lipid handling, inflammatory and oxidative stress pathways, and endothelial homeostasis. In this framework context, downstream consequence mechanisms, including PCSK9 regulation and ferroptosis, are analyzed along with emerging evidence linking estrogen deficiency to modulation of the gut microbiota. The evidence shows the complex interconnections among hormonal, metabolic, and vascular processes underlying postmenopausal atherosclerosis, providing a translational framework for applying therapeutic interventions.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147580970","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

Baicalin Attenuates Oxidative Stress and Apoptosis in Myocardial Ischemia/reperfusion Injury via Suppression of STING/NLRP3 Pathway. 黄芩苷通过抑制STING/NLRP3通路减轻心肌缺血/再灌注损伤的氧化应激和细胞凋亡

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-27 DOI: 10.1007/s12265-026-10765-9

Qi Li, Jiaxin Wang, Yilong Jiang, Fei Wang, Ming Liu, Donghong Yang, Xu Yan, Yue Wang, Haozhen Du, Qingsheng You, Kun Liu

{"title":"Baicalin Attenuates Oxidative Stress and Apoptosis in Myocardial Ischemia/reperfusion Injury via Suppression of STING/NLRP3 Pathway.","authors":"Qi Li, Jiaxin Wang, Yilong Jiang, Fei Wang, Ming Liu, Donghong Yang, Xu Yan, Yue Wang, Haozhen Du, Qingsheng You, Kun Liu","doi":"10.1007/s12265-026-10765-9","DOIUrl":"10.1007/s12265-026-10765-9","url":null,"abstract":"Ischemic heart disease, as one of the major causes of morbidity worldwide, there is no effective therapy for preventing myocardial ischemia-reperfusion injury (MIRI). Baicalin, a flavonoid glycoside extracted from the Scutellaria baicalensis Georgi, yet its effects in MIRI remain unclear. In the study, pretreatment with Baicalin (100 mg/kg, i.p.) markedly alleviated I/R-induced cardiac dysfunction, as shown by reduced serum lactate dehydrogenase (LDH), creatine kinase (CK), and myocardial infarction. Baicalin also improved cardiomyocyte survival by increasing Bcl-2 and decreasing Bax and caspase-3/9 levels. In addition, Baicalin suppressed oxidative stress by reducing malondialdehyde (MDA) while elevating glutathione (GSH) and superoxide dismutase (SOD) levels. Moreover, Baicalin inhibited the STING, NLRP3, cleaved caspase-1, IL-18, and IL-1β expression in vivo and in vitro. Crucially, amidobenzimidazole (ABZI), a STING agonist, reversed the cardioprotective effects of Baicalin. Collectively, these findings demonstrated that Baicalin exerted cardioprotective effects by attenuating apoptosis and oxidative stress through suppression of STING/NLRP3 activation.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147529318","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

ALDH2/eIF3E as Novel Regulators of Cardiac Ferroptosis. ALDH2/eIF3E：心脏铁下垂的新调控因子

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-25 DOI: 10.1007/s12265-026-10767-7

Siqi Wang, Shuqin Liu, Sihui Zang, Tingting Yang, Junjie Xiao

引用次数: 0

The Gut Metabolite Phenylacetylglutamine Inhibits the Angiogenic Potential of Human Umbilical Vein Endothelial Cells Via the β-Adrenergic Receptor-LDHA Axis. 肠道代谢物苯乙酰谷氨酰胺通过β-肾上腺素能受体- ldha轴抑制人脐静脉内皮细胞的血管生成潜能。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-24 DOI: 10.1007/s12265-026-10764-w

Yin Zhang, Wenlong Yang, Jinyan Zhang, Jixiang A, Jinye Shen, Zhiyong Qi, Juying Qian, Aijun Sun, Junbo Ge, Shuning Zhang

{"title":"The Gut Metabolite Phenylacetylglutamine Inhibits the Angiogenic Potential of Human Umbilical Vein Endothelial Cells Via the β-Adrenergic Receptor-LDHA Axis.","authors":"Yin Zhang, Wenlong Yang, Jinyan Zhang, Jixiang A, Jinye Shen, Zhiyong Qi, Juying Qian, Aijun Sun, Junbo Ge, Shuning Zhang","doi":"10.1007/s12265-026-10764-w","DOIUrl":"10.1007/s12265-026-10764-w","url":null,"abstract":"Phenylacetylglutamine (PAGln), a gut microbiota-derived metabolite, is associated with enhanced thrombosis. However, its impact on endothelial function and angiogenesis remains unclear. A murine hindlimb ischemia model was used to assess perfusion recovery. Human umbilical vein endothelial cell (HUVEC) proliferation, migration, and tube formation were evaluated in vitro. Gene set enrichment analysis (GSEA) was performed for pathway enrichment analyses. Furthermore, glycolytic flux and enzyme expression were measured. Lentiviral lactate dehydrogenase A (LDHA) overexpression was performed both in vitro and in vivo. Elevated PAGln impaired blood flow recovery and inhibited HUVEC proliferation, migration and tube formation. β-receptor blocker zenidolol was able to reverse the adverse effects. PAGln downregulated glycolytic pathways, reduced proton efflux, and suppressed LDHA expression and lactate production. LDHA overexpression rescued PAGln-induced angiogenic impairment. The gut metabolite PAGln may suppress angiogenesis of HUVEC by targeting the β-receptors, subseqeuently inhibiting LDHA expression.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13013128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512354","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

The Microbial Mechanisms of Cardiovascular Disease: Oral Dysbiosis as a Systemic Instigator. 心血管疾病的微生物机制：口腔生态失调是一个系统性诱因。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-03-12 DOI: 10.1007/s12265-026-10761-z

Laresh N Mistry, Sumeet Agarwal, Sankalp Dattaram Bhandarkar, Vivek Sharma, Himmat Jaiswal, Saudamini More

引用次数: 0

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 2.6 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":"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":2.6,"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 2.6 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 2.6 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":"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":2.6,"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 2.6 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":2.6,"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