Ayman El-Menyar, Naushad A Khan, Abdul Rehman Abid, Eman Elmenyar, Hassan Al-Thani
{"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":"https://doi.org/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":2.5,"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":"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":"https://doi.org/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":2.5,"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}
Jianing Wang, Yuetong Li, Yuan Liu, Zihui Zhang, Heng Ma
{"title":"Traditional Chinese Medicine Targeting Ferroptosis in Cardiovascular Diseases: Advances and Perspectives.","authors":"Jianing Wang, Yuetong Li, Yuan Liu, Zihui Zhang, Heng Ma","doi":"10.1007/s12265-026-10769-5","DOIUrl":"https://doi.org/10.1007/s12265-026-10769-5","url":null,"abstract":"<p><p>Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation and redox imbalance, has recently garnered significant attention for its critical role in the pathogenesis of cardiovascular diseases (CVDs). Accumulating evidence suggests that ferroptosis contributes to a range of cardiovascular pathologies by disturbing iron homeostasis, promoting oxidative stress, and impairing mitochondrial function. Traditional Chinese medicine (TCM), with its multi-component and multi-target properties and relatively low toxicity, has shown unique therapeutic potential in modulating ferroptosis-related pathways. This review provides a comprehensive summary of the current understanding of ferroptosis in CVDs and highlights the mechanisms by which TCM and its bioactive constituents influence ferroptosis. We further discuss the therapeutic implications and translational challenges, aiming to provide novel insights into ferroptosis-targeted interventions for CVDs from the perspective of TCM.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690433","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}
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":"https://doi.org/10.1007/s12265-026-10766-8","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"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}
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":"https://doi.org/10.1007/s12265-026-10765-9","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"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}
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":"<p><p>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.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"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}
Laresh N Mistry, Sumeet Agarwal, Sankalp Dattaram Bhandarkar, Vivek Sharma, Himmat Jaiswal, Saudamini More
{"title":"The Microbial Mechanisms of Cardiovascular Disease: Oral Dysbiosis as a Systemic Instigator.","authors":"Laresh N Mistry, Sumeet Agarwal, Sankalp Dattaram Bhandarkar, Vivek Sharma, Himmat Jaiswal, Saudamini More","doi":"10.1007/s12265-026-10761-z","DOIUrl":"https://doi.org/10.1007/s12265-026-10761-z","url":null,"abstract":"<p><p>Oral dysbiosis, particularly through periodontal disease, links strongly to cardiovascular risks by driving chronic inflammation and microbial translocation. Key pathogens invade vascular tissues, triggering systemic cytokines and metabolites that damage endothelial function and promote atherosclerosis. This creates a vicious cycle where oral inflammation worsens heart disease progression. Clinical interventions like intensive periodontal therapy show promise, reducing blood pressure and inflammatory markers in at-risk patients, much like established lifestyle changes. Salivary microbial profiles emerge as early warning signs for vascular issues and poor outcomes. This review bridges epidemiology, mechanisms, trials, biomarkers, and practical strategies, clarifying causal gaps through structured evidence analysis. Future multi-omics research and standardized approaches will refine oral health's role in heart disease prevention, offering actionable public health steps.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147443653","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}