Journal of Cardiovascular Translational Research最新文献

{"title":"Psychological Scars and Physical Consequences: Linking PTSD to Cardiovascular Health.","authors":"Alexa Corker, Griffin Oh, Kristine Y DeLeon-Pennell","doi":"10.1007/s12265-026-10783-7","DOIUrl":"10.1007/s12265-026-10783-7","url":null,"abstract":"<p><p>Post traumatic stress disorder (PTSD) is defined as a mental health condition that occurs after experiencing a traumatic event. Patients diagnosed with PTSD have a 30-45% increase in cardiovascular disease (CVD) risk or cardiac-specific mortality even after adjusting for depression, demographic, clinical (e.g., age, blood pressure, body mass index (BMI), and tobacco use), and psychosocial factors. With this, the lifetime prevalence of PTSD has a notable sex disparity: women have a prevalence of approximately 10%, compared to 4% in men. Mechanisms explaining the increased risk of CVD in PTSD patients is unclear, leaving this patient population vulnerable as well as placing a substantial economic burden on the United States healthcare system. In this review, we will discuss the effect of PTSD on cardiovascular physiology, with an emphasis on sex differences, mechanisms of inflammation, and impaired ANS responses. In addition, we will summarize current and experimental therapeutics for PTSD that may help mitigate the risk of CVD.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148031043","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}

{"title":"Persistent Proteomic Signatures in Takotsubo Syndrome: Methodological Considerations Regarding Reference Cohort Selection and Confounding.","authors":"Fatih Aydin","doi":"10.1007/s12265-026-10786-4","DOIUrl":"10.1007/s12265-026-10786-4","url":null,"abstract":"","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030985","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":"Iron Deficiency Screening in Patients Admitted with Acute Heart Failure Decompensation.","authors":"Alex M Sindledecker, Yassar Nabeel, Olivia Palladino, Lawrence A Frazee","doi":"10.1007/s12265-026-10774-8","DOIUrl":"10.1007/s12265-026-10774-8","url":null,"abstract":"<p><p>Correction of iron deficiency (ID) with intravenous iron among patients with heart failure (HF) may improve outcomes but is rarely assessed in real-world studies. Hospital admission for decompensated HF presents an opportunity to identify patients for treatment of ID. Of 2,275 patient admissions for decompensated HF, iron studies were available for 526 (23.1%) and ID was identified in 332 (63.1%) patients. Iron replacement was oral in 241 (10.6%) or intravenous in 285 (12.5%) with 132 (46.3%) patients receiving treatment during the admission. Anemia, chronic kidney disease stage 3 (CKD3), and low mean corpuscular volume (MCV) were associated with a higher odds of iron study availability while age was associated with lower odds. Frequency of assessment of ID in HF patients remains low. Predictors of iron status assessment indicate that factors related to anemia rather than HF are likely responsible for iron status assessment among these patients.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972835","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}

{"title":"Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5.","authors":"Xiang-Bo An, Yi-Tong Wang, Xin Liu, Fei Gao, Zhi-Jian Wang","doi":"10.1007/s12265-026-10777-5","DOIUrl":"10.1007/s12265-026-10777-5","url":null,"abstract":"<p><p>Pathological cardiac hypertrophy is a key precursor to heart failure. The role of Xanthatin in this process was unknown. This study aimed to investigate its effects and molecular target. A mouse model of Ang II-induced hypertrophy was used. Xanthatin's effects were assessed by echocardiography and histology. Cardiac-specific overexpression or knockdown of CREB5 was performed using AAV9-cTNT vectors during Ang II and Xanthatin co-treatment to validate its functional role. Xanthatin treatment significantly alleviated Ang II-induced cardiac hypertrophy, oxidative stress, fibrosis, and inflammation. Crucially, cardiac-specific overexpression of CREB5 markedly attenuated these protective effects of Xanthatin. Conversely, cardiac-specific knockdown of CREB5 synergized with Xanthatin, further enhancing its suppressive actions on all pathological hallmarks. Xanthatin is a potent inhibitor of Ang II-induced cardiac hypertrophy, and its protective effect is mediated through the suppression of CREB5 signaling. This identifies the Xanthatin-CREB5 axis as a novel and promising therapeutic target for pathological cardiac remodeling.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972832","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":"Ventricle-Specific Biomechanical Responses to Inotropic and Vasoactive Drugs in Human Myocardial Slices.","authors":"Sanne J J Langmuur, Jorik H Amesz, Rahi S Alipour Symakani, Kevin M Veen, Christiaan L Meuwese, Ad J J C Bogers, Natasja M S de Groot, Olivier C Manintveld, Yannick J H J Taverne","doi":"10.1007/s12265-026-10773-9","DOIUrl":"10.1007/s12265-026-10773-9","url":null,"abstract":"<p><p>This study aimed to compare baseline biomechanical contractile properties between right (RV) and left ventricular (LV) human living myocardial slices (LMS) and explore the effect of dobutamine, noradrenaline, adrenaline, levosimendan and enoximone in both ventricles. Sixty-three slices (33 RV, 30 LV) were produced from 5 explanted hearts. At baseline, RV LMS had a higher maximum contraction force, shorter contraction duration, time to peak and time to relaxation, steeper dF/dt and a larger peak area than LV LMS. Dobutamine administration had a larger effect in RV than LV LMS. Spontaneous, irregular contractions were observed after noradrenaline, adrenaline and dobutamine administration. In conclusion, RV LMS showed a stronger contraction with higher contraction velocity as compared to LV LMS and exhibited a greater response to dobutamine. These findings contribute to the understanding of the RV physiology as a separate entity, advocating for a different approach in treating RV or LV dysfunction.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13160974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874343","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}

{"title":"Targeting Siglec-E Modulates Macrophage Polarization to Attenuate Cardiac Remodeling After Myocardial Infarction.","authors":"Yuan Li, Yuyang Chen, Jing Yang, Bifang Mai, Jun Chen, Jingfeng Wang, Shuanglun Xie","doi":"10.1007/s12265-026-10771-x","DOIUrl":"10.1007/s12265-026-10771-x","url":null,"abstract":"<p><p>Adverse cardiac remodeling after myocardial infarction (MI) is a major cause of heart failure. Macrophage polarization plays a pivotal role in this process. Siglec-E, an immunoregulatory molecule expressed on myeloid cells, modulates macrophage function, yet its specific role in post-MI cardiac remodeling remains unknown. Elucidating this role may reveal novel therapeutic strategies and provide critical safety insights for Siglec-E-targeted anticancer therapies. Siglec-9 (the human homolog of Siglec-E) expression was first identified in GEO datasets and validated by flow cytometry in a human cohort (AMI,controls,and CCS). Siglec-E expression was then examined in murine models of MI. To assess its functional role, Siglec-E⁻/⁻ and wild-type mice were subjected to permanent coronary artery ligation. Cardiac remodeling was evaluated by echocardiography and histopathological examination. Immune cell profiles, macrophage polarization, and inflammatory gene expression were analyzed by flow cytometry,immunofluorescence, and qPCR. Finally, macrophage depletion and adoptive transfer studies were performed to establish causality. Siglec-9/E expression was upregulated in monocytes/macrophages after MI in human and mice. Compared to WT controls, Siglec-E⁻/⁻ mice exhibited worsened survival, impaired cardiac function (reduced left ventricular ejection fraction and fractional shortening, increased ventricular volumes), larger infarct size, exacerbated fibrosis, and enhanced cardiomyocyte apoptosis after MI. Mechanistically, Siglec-E deficiency skewed cardiac macrophages toward a pro-inflammatory M1 phenotype, without affecting neutrophil recruitment. Macrophage depletion abolished the adverse phenotype in Siglec-E⁻/⁻ mice. Adoptive transfer of wild-type macrophages attenuated cardiac injury, whereas transfer of Siglec-E⁻/⁻ macrophages exacerbated adverse remodeling. Siglec-E is a key regulator of post-MI cardiac remodeling by restraining pro-inflammatory M1 macrophage polarization. Targeting macrophage Siglec-E signaling may represent a promising therapeutic strategy for heart failure.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868613","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":"HNMT: A Key Pro-hypertrophic Factor in Pressure Overload.","authors":"Hang Chen, Yifu Chen, Shihui Zang, Xuerui Chen, Junjie Xiao","doi":"10.1007/s12265-026-10775-7","DOIUrl":"10.1007/s12265-026-10775-7","url":null,"abstract":"","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147815451","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":"Scoping Review on True and Relative Bradycardia in Trauma: How to Approach Bradycardia in Traumatic Brain Injury.","authors":"Ayman El-Menyar, Naushad A Khan, Abdul Rehman Abid, Eman Elmenyar, Hassan Al-Thani","doi":"10.1007/s12265-026-10772-w","DOIUrl":"10.1007/s12265-026-10772-w","url":null,"abstract":"<p><p>Brain-heart interactions have garnered considerable interest in the landscape of traumatic brain injury (TBI). This scoping review focused on bradycardia caused by high intracranial pressure (ICP), brainstem injury, autonomic imbalance, hypothalamic-pituitary-adrenal axis disruption, or massive bleeding. The latter condition is attributed to a physiological phenomenon called relative bradycardia (RB). True bradycardia results from underlying physiological or pathological cardiac disorders, whereas RB has different definitions and implications in medical and surgical settings. The former reflects pulse-temperature dissociation, while the latter reflects pulse-pressure dissociation. However, it can reflect an abnormal neurological response called the Cushing reflex. Therefore, bradycardia may indicate imminent shock after TBI associated with torso injuries or high ICP following severe isolated TBI. RB is underrecognized and underappreciated in emergency settings. This review investigated whether RB affects patient survival and neurological function. Physicians should approach patients presenting with RB with a high index of suspicion and timely management.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772590","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}

{"title":"Nuclear eNOS-ADAR1 Signaling in Endothelial Immunoregulation.","authors":"Siqi Wang, Yifu Chen, Shihui Zang, Tingting Yang, Junjie Xiao","doi":"10.1007/s12265-026-10770-y","DOIUrl":"10.1007/s12265-026-10770-y","url":null,"abstract":"","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716886","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":"New Advances in the Mechanisms and Therapeutic Strategies of Gut Microbiota in Regulating Glycolipid Metabolism to Combat Atherosclerosis.","authors":"Hui Zhang, Pihong Liu, Naizhi Geng","doi":"10.1007/s12265-026-10768-6","DOIUrl":"10.1007/s12265-026-10768-6","url":null,"abstract":"<p><p>Atherosclerosis is the major pathological basis of cardiovascular diseases, characterized by chronic inflammation and disturbed glucose and lipid metabolism. Despite the widespread use of statins, the global clinical burden continues to rise, and effective therapeutic strategies remain limited. As the \"second genome,\" gut microbiota participates in the progression of atherosclerosis by regulating host glucose and lipid metabolism, inflammatory responses, and metabolite production. Natural plant components exert multiple effects, including regulating glucose and lipid metabolism, modulating gut microbiota, and anti-inflammatory activity, showing unique advantages in the prevention and treatment of atherosclerosis. This review summarizes the mechanisms underlying the anti-atherosclerotic effects of gut microbiota via regulating glucose and lipid metabolism, as well as the role of natural plant components in intervening disease progression by remodeling intestinal microecology and reducing pro-atherogenic metabolites. It provides a theoretical basis for novel therapeutic strategies targeting gut microbiota and the clinical application of plant components.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690492","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}