Faridun Rahimi, Nikolaus Löffelhardt, Jan Minners, Philipp Breitbart, Kilian Franke, Tau Sarra Hartikainen, Christian Valina, Constantin V Zur Mühlen, Thomas Nührenberg, Adnan Kastrati, Felix Woitek, Albrecht Elsaesser, Mohamed Abdel-Wahab, Samuel Sossalla, Willibald Hochholzer, Dirk Westermann, Franz-Josef Neumann, Christoph Olivier, Miroslaw Ferenc
{"title":"Randomised Comparison of Culotte- versus Double Kissing Crush Stenting in de novo non-left Main Coronary Bifurcation Lesions: Rationale and Design of the Bifurcation Bad Krozingen trial-3 (BBK-3).","authors":"Faridun Rahimi, Nikolaus Löffelhardt, Jan Minners, Philipp Breitbart, Kilian Franke, Tau Sarra Hartikainen, Christian Valina, Constantin V Zur Mühlen, Thomas Nührenberg, Adnan Kastrati, Felix Woitek, Albrecht Elsaesser, Mohamed Abdel-Wahab, Samuel Sossalla, Willibald Hochholzer, Dirk Westermann, Franz-Josef Neumann, Christoph Olivier, Miroslaw Ferenc","doi":"10.1007/s12265-025-10626-x","DOIUrl":"https://doi.org/10.1007/s12265-025-10626-x","url":null,"abstract":"<p><p>Whether culotte or double kissing (DK)-crush stenting is the superior systematic 2-stent technique in non-left main bifurcation lesions is unclear. The BBK-3 (unique identifier NCT04192760) is a multicenter, prospective, randomized controlled trial to test the hypothesis that culotte stenting reduces maximal percent diameter restenosis at 9-month follow-up compared to DK-crush stenting in de-novo non-left main coronary bifurcation lesions using approved, third-generation drug-eluting stents (DES). A total of 400 patients will be randomized in a 1:1 ratio to receive a two-stent strategy. The primary study endpoint is the maximal percent diameter in-stent restenosis within the bifurcation at 9 months, assessed by quantitative coronary angiography. Secondary endpoints include target lesion revascularization (TLR), the composite of death and myocardial infarction, emergent cardiac bypass surgery and TLR (MACE) at 12 months. BBK-3 will assist in the identification of the preferable, contemporary 2-stent strategy in the treatment of de-novo non-left main coronary bifurcation lesions.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144159243","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}
Michaël Racodon, Claudine Fabre, Pierre Vanhove, Jordan Do Vale, Romain Bolpaire, Elodie Moutailler, Félicité Malanda, Amandine Secq
{"title":"Validity and Reproducibility of the Six-Minute Stepper Test in Cardiac Patients.","authors":"Michaël Racodon, Claudine Fabre, Pierre Vanhove, Jordan Do Vale, Romain Bolpaire, Elodie Moutailler, Félicité Malanda, Amandine Secq","doi":"10.1007/s12265-025-10624-z","DOIUrl":"https://doi.org/10.1007/s12265-025-10624-z","url":null,"abstract":"<p><p>The Six-Minute Walk Test (6MWT) traditionally assesses exercise capacity in cardiac patients but requires a large space. The Six-Minute Stepper Test (6MST) has been validated as an alternative in various populations. This study evaluates the reproducibility, sensitivity, and validity of the 6MST in 60 cardiac patients (15 women, 45 men, 58 ± 11.2 years). Participants underwent cardiopulmonary exercise tests (CPET), two 6MSTs, and one 6MWT at the start and end of cardiac rehabilitation (CR). Performance in the 6MST improved significantly after CR (343 ± 89.0 vs. 451 ± 105.6 steps, p < 0.0001). The 6MST showed moderate correlation with the 6MWT and CPET (r = 0.54, p < 0.0001). Dyspnoea and leg fatigue were higher in the 6MST than in the 6MWT (p < 0.0001). Conclusion: The 6MST is a safe, valid, sensitive, and reproducible tool for evaluating exercise capacity in cardiac patients, comparable to the 6MWT.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992862","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}
Bifang Mai, Wenlong Jiang, Jing Yang, Yuyang Chen, Zhen Qin, Yuan Li, Wenqing Tu, Yuhan Lin, Wai Seng Chan, Jianhua Wu, Fangzhou Cheng, Tao Xu, Shuanglun Xie
{"title":"Plasma Small Extracellular Vesicles of Ischemic Cardiomyopathy Aggravate Ventricular Remodeling Post-Myocardial Infarction and Promote miR-223-3p-mediated Dysfunction in Regulatory T Cells.","authors":"Bifang Mai, Wenlong Jiang, Jing Yang, Yuyang Chen, Zhen Qin, Yuan Li, Wenqing Tu, Yuhan Lin, Wai Seng Chan, Jianhua Wu, Fangzhou Cheng, Tao Xu, Shuanglun Xie","doi":"10.1007/s12265-025-10623-0","DOIUrl":"https://doi.org/10.1007/s12265-025-10623-0","url":null,"abstract":"<p><p>Treg dysfunction in ischemic cardiomyopathy (ICM) remains mechanistically unclear. We investigated ICM plasma small extracellular vesicles (ICM-sEVs) in Treg regulation and post-MI remodeling. Flow cytometry assessed Treg frequency. ICM-sEV miRNA sequencing revealed miR-223-3p enrichment, validated using miR-223<sup>-/-</sup> and Foxp3<sup>GFP/+</sup> mice. ICM patients and mice exhibited elevated Treg numbers but suppressed Foxp3. miR-223-3p was upregulated in ICM-sEVs and inversely correlated with functional Tregs. ICM-sEVs administration aggravated ventricular remodeling post myocardial infarction (MI) in mice while reducing Treg frequency and elevating miR-223-3p in vitro. miR-223 knockdown increased Treg cell number and Foxp3 expression, whereas miR-223 overexpression reversed the phenotype. ICM-sEVs aggravate ventricular remodeling post-MI and promote miR-223-3p-mediated Treg cell dysfunction.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025544","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}
Yating Zhou, Yanyu Chen, Yuting Cui, Ni Gan, Qiong Xiang, Man Li, Wen Zeng, Xi-Long Zheng, Xiaoyan Dai, Juan Peng, Zhihan Tang
{"title":"Inhibition of VSMC Ferroptosis Mitigates Pathological Vascular Remodeling: A Novel Therapeutic Strategy for Abdominal Aortic Aneurysm.","authors":"Yating Zhou, Yanyu Chen, Yuting Cui, Ni Gan, Qiong Xiang, Man Li, Wen Zeng, Xi-Long Zheng, Xiaoyan Dai, Juan Peng, Zhihan Tang","doi":"10.1007/s12265-025-10621-2","DOIUrl":"https://doi.org/10.1007/s12265-025-10621-2","url":null,"abstract":"<p><p>Ferroptosis plays a key role in abdominal aortic aneurysm (AAA) development. This study explores whether and how ferroptosis regulates AAA progression. Ferroptosis was confirmed in human AAA tissue. In vitro experiments with primary mouse vascular smooth muscle cells (VSMCs) and abdominal aortic rings revealed that angiotensin II (Ang II) triggered ferroptosis in VSMCs. Ferrostatin-1 (Fer-1), a potent ferroptosis inhibitor, effectively suppressed this effect. Additionally, the ferroptosis inducer erastin and Ang II can both promoted pathological remodeling of abdominal aortic rings, but Fer-1 significantly suppressed these effects. In AAA mouse model, Fer-1 treatment reduced AAA formation. Mechanistically, RNA-sequencing analysis revealed that Fer-1 regulates VSMC contractile function, suppresses inflammation, and mitigates extracellular matrix remodeling. These findings highlight the critical role of VSMC ferroptosis in AAA pathogenesis and demonstrate that ferroptosis inhibition effectively reduces pathological vascular remodeling, making it a promising therapeutic strategy for preventing AAA.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965697","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}
Tao Wang, Ziyu Su, Ming Zhong, Xuanqin Wu, Liang Li, Hong Gu, Yunhan Sun, Jun Ji, Xingchun Peng
{"title":"A Metabolic Signature Specific to the Patients with Type 2 Diabetes and its Association with the Pathogenesis of Diabetic-Foot Syndrome.","authors":"Tao Wang, Ziyu Su, Ming Zhong, Xuanqin Wu, Liang Li, Hong Gu, Yunhan Sun, Jun Ji, Xingchun Peng","doi":"10.1007/s12265-025-10622-1","DOIUrl":"https://doi.org/10.1007/s12265-025-10622-1","url":null,"abstract":"<p><p>Oxidative stress and protein nonenzymatic glycation are key factors in diabetic-foot syndrome pathogenesis. Type 2 diabetes (T2DM) progression involves excessive gluconolactone (GDL) production, linked to endothelial injury and diabetic arteriosclerosis. This study explored GDL's role in diabetic-foot syndrome using high-performance liquid chromatography-tandem mass spectrometry to analyze sera from 75 T2DM patients (including 32 with diabetic-foot) and 36 healthy controls. GDL levels were significantly higher in T2DM patients and correlated with increased hemoglobin A1c glycation and reactive oxygen species production in endothelial cells, suggesting GDL's role in accelerating macrovascular arteriosclerosis and diabetic-foot syndrome. These findings highlight GDL's potential as a diagnostic biomarker and therapeutic target for diabetic macrovascular complications.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143994617","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":"Glycerophospholipid and Sphingosine- 1-phosphate Metabolism in Cardiovascular Disease: Mechanisms and Therapeutic Potential.","authors":"Huiru Tang, Chengxia Kan, Kexin Zhang, Sufang Sheng, Hongyan Qiu, Yujie Ma, Yuqun Wang, Ningning Hou, Jingwen Zhang, Xiaodong Sun","doi":"10.1007/s12265-025-10620-3","DOIUrl":"https://doi.org/10.1007/s12265-025-10620-3","url":null,"abstract":"<p><p>Cardiovascular disease remains a leading cause of mortality worldwide, driven by factors such as dysregulated lipid metabolism, oxidative stress, and inflammation. Recent studies highlight the critical roles of both glycerophospholipid and sphingosine- 1-phosphate metabolism in the pathogenesis of cardiovascular disorders. However, the contributions of glycerophospholipid-derived metabolites remain underappreciated. Glycerophospholipid metabolism generates bioactive molecules that contribute to endothelial dysfunction, lipid accumulation, and cardiac cell injury while also modulating inflammatory and oxidative stress responses. Meanwhile, sphingosine- 1-phosphate is a bioactive lipid mediator that regulates vascular integrity, inflammation, and cardiac remodeling through its G-protein-coupled receptors. The convergence of these pathways presents novel therapeutic opportunities, where dietary interventions such as omega- 3 polyunsaturated fatty acids and pharmacological targeting of sphingosine- 1-phosphate receptors could synergistically mitigate cardiovascular risk. This review underscores the need for further investigation into the interplay between glycerophospholipid metabolism and sphingosine- 1-phosphate signaling to advance targeted therapies for the prevention and management of cardiovascular disease.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025421","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":"Connecting the Dots: Stress Granule and Cardiovascular Diseases.","authors":"Gaowei Yang, Yiming Wang, Junfang Guo, Tao Rui","doi":"10.1007/s12265-025-10619-w","DOIUrl":"https://doi.org/10.1007/s12265-025-10619-w","url":null,"abstract":"<p><p>Stress granules (SGs) are membrane-less cytoplasmic assemblies composed of mRNAs and RNA-binding proteins (RBPs) that transiently form to cope with various cellular stressors by halting mRNA translation and, consequently, protein synthesis. SG formation plays a crucial role in regulating multiple cellular processes, including cellular senescence, inflammatory responses, and adaptation to oxidative stress under both physiological and pathological conditions. Dysregulation of SG assembly and disassembly has been implicated in the pathogenesis of various diseases, including cardiovascular diseases (CVDs), cancer, viral and bacterial infections, and degenerative diseases. In this review, we survey the key aspects of SGs biogenesis and biological functions, with a particular focus on their causal involvement in CVDs. Furthermore, we summarized several SG-modulating compounds and discussed the therapeutic potential of small molecules targeting SG-related diseases in clinical settings.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009106","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}
Mohsen Davari, Mahmoud Khansari, Sahar Hosseini, Reza Morovatshoar, Alireza Azani, Seyedeh Tarlan Mirzohreh, Mohammadjavad Ashrafi Mahabadi, Moein Ghasemi, Mohammad Saeed Soleimani Meigoli, Sima Foroughi Nematollahi, Sina Pourranjbar, Qumars Behfar, Mandana Baghdadi, Ahmad Mir Hosseini
{"title":"The Impact of Opioids on Epigenetic Modulation in Myocardial Ischemia and Reperfusion Injury: Focus on Non-coding RNAs.","authors":"Mohsen Davari, Mahmoud Khansari, Sahar Hosseini, Reza Morovatshoar, Alireza Azani, Seyedeh Tarlan Mirzohreh, Mohammadjavad Ashrafi Mahabadi, Moein Ghasemi, Mohammad Saeed Soleimani Meigoli, Sima Foroughi Nematollahi, Sina Pourranjbar, Qumars Behfar, Mandana Baghdadi, Ahmad Mir Hosseini","doi":"10.1007/s12265-025-10609-y","DOIUrl":"https://doi.org/10.1007/s12265-025-10609-y","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion injury (IRI) is a major issue in cardiovascular medicine, marked by tissue damage from the restoration of blood flow after ischemia. Opioids, known for their pain-relieving properties, have emerged as potential cardioprotective agents in IRI. Recent research suggests opioids influence epigenetic mechanisms-such as histone modifications and non-coding RNAs (ncRNAs)-which are essential for regulating gene expression and cellular responses during myocardial IRI. This review delves into how opioids like remifentanil affect histone modifications, DNA methylation, and ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Remifentanil postconditioning (RPC) reduces apoptosis in cardiomyocytes through histone deacetylation, specifically downregulating histone deacetylase 3 (HDAC3). Similarly, opioids impact miRNAs such as miR- 206 - 3p and miR- 320 - 3p, and lncRNAs like TINCR and UCA1, which influence apoptosis, inflammation, and oxidative stress. Understanding these interactions highlights the potential for opioid-based therapies in mitigating IRI-induced myocardial damage.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811529","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":"CRISPR-Cas9 Targeting PCSK9: A Promising Therapeutic Approach for Atherosclerosis.","authors":"Bin Gu, Min Li, Dan Li, Kaisen Huang","doi":"10.1007/s12265-024-10587-7","DOIUrl":"10.1007/s12265-024-10587-7","url":null,"abstract":"<p><p>CRISPR-Cas9 gene editing technology, as an innovative biomedical tool, holds significant potential in the prevention and treatment of atherosclerosis. By precisely editing key genes such as PCSK9, CRISPR-Cas9 offers the possibility of long-term regulation of low-density lipoprotein cholesterol (LDL-C), which may reduce the risk of cardiovascular diseases. Early clinical studies of gene editing therapies like VERVE-101 have yielded encouraging results, highlighting both the feasibility and potential efficacy of this technology. However, clinical applications still face challenges such as off-target effects, immunogenicity, and long-term safety. Future research should focus on enhancing the specificity and efficiency of gene editing, optimizing delivery systems, and improving personalized treatment strategies. Additionally, the establishment of ethical and legal regulatory frameworks will be critical for the safe adoption of this technology. With the continued advancement of gene editing technology, CRISPR-Cas9 may become an important tool for treating atherosclerosis and other complex diseases.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"424-441"},"PeriodicalIF":2.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970956","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}
Lin Lin, Jin Wei, Jiahong Xue, Gang Fan, Wenjing Zhu, Yanhe Zhu, Ruiyun Wu
{"title":"Drp1 Promotes Macrophage M1 Polarization and Inflammatory Response in Autoimmune Myocarditis by Driving Mitochondrial Fission.","authors":"Lin Lin, Jin Wei, Jiahong Xue, Gang Fan, Wenjing Zhu, Yanhe Zhu, Ruiyun Wu","doi":"10.1007/s12265-024-10570-2","DOIUrl":"10.1007/s12265-024-10570-2","url":null,"abstract":"<p><p>Autoimmune myocarditis (AM) is characterized by an intricate inflammatory response within the myocardium. Dynamin-related protein 1 (Drp1), a pivotal modulator of mitochondrial fission, plays a role in the pathogenesis of various diseases. A myosin-induced experimental autoimmune myocarditis (EAM) mouse model was successfully established. Flow cytometry was employed to detect M1/M2-like macrophages. Mitochondrial fragmentation was assessed using Mito-Tracker Red CMXRos. Drp1 was upregulated and activated in EAM mice. Depletion of Drp1 was observed to mitigate inflammation, macrophage infiltration and M1 polarization within the cardiac tissue of EAM mice. In M1-like macrophages derived from the hearts of EAM mice, Drp1 was found to promote mitochondrial fission and diminish mitochondrial fusion. Furthermore, the depletion of Drp1 reduced the NF-κB-related pro-inflammatory response in EAM-associated M1-like macrophages. Drp1 drives mitochondrial fission in macrophages, driving their M1 polarization and the subsequent inflammatory response. Drp1 may represent an effective target for the prevention and treatment of AM.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"237-246"},"PeriodicalIF":2.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400328","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}