Cardiovascular Diabetology最新文献

{"title":"Causal association of modifiable factors with cardiometabolic multimorbidity: an exposome-wide Mendelian randomization investigation.","authors":"Dun Li, Jing Lin, Hongxi Yang, Lihui Zhou, Yujian Li, Zhe Xu, Li Sun, Xinyu Zhang, Weili Xu, Yaogang Wang","doi":"10.1186/s12933-025-02790-w","DOIUrl":"10.1186/s12933-025-02790-w","url":null,"abstract":"<p><strong>Background: </strong>Cardiometabolic multimorbidity (CMM), characterized by the co-existence of two or more cardiometabolic diseases (CMDs) including type 2 diabetes (T2D), coronary artery disease (CAD), and stroke, persists as a global health challenge. However, the causal associations of modifiable factors with CMDs and CMM remains to be systematically investigated.</p><p><strong>Methods: </strong>In this study, a three-stage design Mendelian randomization (MR) investigation was conducted, using two-sample MR with potential sample overlap correction and multiple testing, multivariable MR analysis, and multi-response MR, with modifiable factors covering domains of socioeconomic factors, behavioral factors, biochemical factors, and physical measures as exposures, and CMM and CMDs as outcomes. Updated large-scale genome-wide association study (GWAS) data based on systematic collection from GWAS Catalog were applied.</p><p><strong>Results: </strong>Our major findings suggested that, 13 of 23 modifiable factors across four domains, including educational attainment (odds ratio: 0.858, 95% confidence interval: 0.834-0.883), household income (0.794, 0.720-0.875), lifetime smoking behavior (1.201, 1.145-1.260), leisure screen time (1.255, 1.186-1.327), low-density lipoprotein cholesterol levels (1.062, 1.046-1.079), total cholesterol levels (1.045, 1.029-1.062), Apolipoprotein B (1.035, 1.019-1.051), fasting glucose (1.096, 1.038-1.157), glycated hemoglobin (HbA1c) (1.062, 1.037-1.089), systolic blood pressure (1.125, 1.104-1.146), diastolic blood pressure (1.104, 1.083-1.126), forced expiratory volume in 1 s (FEV₁) (0.953, 0.931-0.975), and body mass index (BMI) (1.243, 1.210-1.277) were evaluated with relatively robust effects on CMM. Furthermore, household income, lifetime smoking behavior, HbA1c, systolic blood pressure, and FEV₁ with CMM were detected as independent associations within a single domain. Similar results were observed in each CMD. Moreover, the multi-response MR provided reinforcing evidence for the associations of educational attainment, serum urate, and BMI with CMM, and lifetime smoking behavior, moderate to vigorous intensity physical activity, and leisure screen time with diverse CMDs.</p><p><strong>Conclusions: </strong>Promoting educational attainment, maintaining favorable serum urate, and controlling obesity are specifically prioritized for CMM prevention. Furthermore, avoiding smoking and sedentary behavior, and strengthening physical activity held prominent protective impacts on CMDs. Additionally, improving dyslipidemia and dysglycemia, maintaining favorable blood pressure, and enhancing lung function, would contribute to the co-management of CMDs and preventing the long-term CMM condition. Our investigation provided causality-oriented evidence to establish the risk profile of CMM.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"241"},"PeriodicalIF":8.5,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment with orforglipron, an oral glucagon like peptide-1 receptor agonist, is associated with improvements of CV risk biomarkers in participants with type 2 diabetes or obesity without diabetes.","authors":"Sean Wharton, Julio Rosenstock, Manige Konige, Yanzhu Lin, Kevin Duffin, Jonathan Wilson, Hiya Banerjee, Valentina Pirro, Christof Kazda, Kieren Mather","doi":"10.1186/s12933-025-02781-x","DOIUrl":"10.1186/s12933-025-02781-x","url":null,"abstract":"<p><strong>Background: </strong>Orforglipron, a novel oral, non-peptide glucagon like peptide-1 (GLP-1) receptor agonist, has demonstrated efficacy in improving body weight reduction and glycemic control. However, its potential benefits in improving cardiovascular (CV) risk factors have yet to be determined. We assessed the effect of orforglipron in participants with type 2 diabetes (T2D) and/or overweight or obesity on blood pressure, lipid, and inflammatory biomarkers associated with risk for major adverse cardiovascular events.</p><p><strong>Methods: </strong>Using data from participants with available samples from Phase 2 trials of orforglipron in participants with T2D (N = 361) or with overweight or obesity without diabetes mellitus (N = 234), we performed an exploratory analysis of changes in CV risk markers. For the T2D study, participants mean age 59 years, 40% were assigned female at birth with a mean HbA_1c of 8.1% and mean BMI of 35.3 kg/m²; they received once daily orforglipron doses (3, 12, 24, 36, or 45 mg) or once weekly subcutaneous dulaglutide 1.5 mg, or placebo. In the obesity study, participants had a mean age 54 years, 60% were assigned female at birth, and mean BMI was 37.9 kg/m²; they received once daily orforglipron (12, 24, 36, or 45 mg) or placebo. The change from baseline at 26 weeks (T2D study) or 36 weeks (obesity study) in blood pressure, lipids (cholesterol, triglycerides, Apolipoprotein B (ApoB), Apolipoprotein C3 (ApoC3), N-terminal pro-b-type natriuretic peptide (NT-pro-BNP), and inflammatory biomarkers (high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6)) were assessed.</p><p><strong>Results: </strong>Significant placebo-adjusted decreases from baseline in blood pressure, low-density lipoprotein (LDL) cholesterol, triglycerides, ApoB, ApoC3, and hsCRP were observed following orforglipron treatment in participants with T2D and/or overweight or obesity. In both studies, improvements in blood pressure, lipid parameters, and most of the evaluated biomarkers were of similar magnitude after treatment with 12 mg orforglipron as with 24, 36, and 45 mg.</p><p><strong>Conclusion: </strong>Orforglipron treatment was associated with beneficial changes in CV risk markers in participants with T2D and in participants with overweight/obesity without T2D. (Clinicaltrials.gov: NCT05048719, NCT05051579).</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"240"},"PeriodicalIF":8.5,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12142847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-specific cardiometabolic multimorbidity, metabolic syndrome and left ventricular function in heart failure with preserved ejection fraction in the UK Biobank.","authors":"Ambre Bertrand, Xin Zhou, Andrew Lewis, Thomas Monfeuga, Ramneek Gupta, Vicente Grau, Blanca Rodriguez","doi":"10.1186/s12933-025-02788-4","DOIUrl":"10.1186/s12933-025-02788-4","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Cardiometabolic disturbances play a central role in the pathogenesis of heart failure with preserved ejection fraction (HFpEF). Due to its complexity, HFpEF is a challenging condition to treat, making phenotype-specific disease management a promising approach. However, HFpEF phenotypes are heterogenous and there is a lack of detailed evidence on the different, sex-specific profiles of cardiometabolic multimorbidity and metabolic syndrome present in HFpEF.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We performed a retrospective, modified cross-sectional study examining a subset of participants in the UK Biobank, an ongoing multi-centre prospective cohort study in the United Kingdom. We defined HFpEF as a record of a heart failure diagnosis using ICD-10 code I50, coupled with a left ventricular ejection fraction (LVEF) ≥ 50% derived from cardiac magnetic resonance (CMR) imaging. We examined sex-specific differences in cardiometabolic comorbidity burden and metabolic syndrome, performed latent class analysis (LCA) to identify distinct clusters of patients based on their cardiometabolic profile, and compared CMR imaging-derived parameters of left ventricular function at rest in the different clusters identified to reflect possible differences in adverse cardiac remodelling.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We ascertained HFpEF in 445 participants, of which 299 (67%) were men and 146 (33%) women. The median age was 70 years old (interquartile range: [66.0-74.0]). A combination of hypertension and obesity was the most prevalent cardiometabolic pattern both in men and women with HFpEF. Most men had 2-3 clinical cardiometabolic comorbidities while most women had 1-2, despite a similar metabolic syndrome profile (p = 0.05). LCA revealed three distinct, clinically relevant phenogroups, namely (1) a most male and multimorbid group (n = 117); (2) a group with a high prevalence of severe obesity, abnormal waist circumference and with the highest relative proportion of females (n = 116); and finally (3) a group with an apparently lower comorbidity burden aside from hypertension (n = 212). There were significant differences in clinical measurements and medication across the three phenogroups identified. Cardiac output at rest was significantly higher in group 2 vs. group 3 (males: median 5.6 L/min vs. 5.2 L/min, p &lt; 0.05; females: 5.1 L/min vs. 4.4 L/min, p &lt; 0.01). Absolute global longitudinal strain was significantly lower in women in group 1 vs. group 2 (-17.6% vs. -18.5%, p &lt; 0.05).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Women with cardiometabolic HFpEF had a lower comorbidity burden compared to men despite a similar metabolic syndrome profile. Based on patients' cardiometabolic profile, we identified three distinct subgroups which differed in body shape and mass, lipid biomarker and medication profile, as well as in cardiac output at rest both in men and women. These factors may affect disease trajectory, treatment options and outcomes in th","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"238"},"PeriodicalIF":8.5,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pseudohypoxia caused by germline genetic alterations in the VHL gene is associated with increased diabetes and cardiovascular risk: a UK biobank study.","authors":"Reut Halperin, Roi Horwitz, Yair Schwarz, Amit Tirosh","doi":"10.1186/s12933-025-02799-1","DOIUrl":"10.1186/s12933-025-02799-1","url":null,"abstract":"<p><strong>Background: </strong>Von Hippel-Lindau protein deficiency leads to cellular and tissue false sense of hypoxia (pseudohypoxia), driving erythropoiesis, angiogenesis, and dysglycemia. The impact of partial VHL protein deficiency, caused by heterozygous VHL gene alterations on diabetes and cardiovascular risk has not been investigated. Hence, in the current study we assessed a possible association between VHL genotype and cardiovascular risk based on a the UK Biobank genomic and clinical data.</p><p><strong>Methods: </strong>Demographic, clinical and biochemical data were extracted, and exome analysis, focusing on the VHL gene locus was performed for all patients (n = 460,430). Variant severity was sub-categorized into low (5'- and 3'-untranslated region (UTR)), medium (missense, in-frame indels), and high-risk (nonsense, splice-site, and frameshift). Metabolic and cardiovascular outcomes were compared between VHL variant carriers vs. non-carriers.</p><p><strong>Results: </strong>VHL gene variant carriers (n = 2516) had an increased risk of diabetes (p = 0.04) and cerebrovascular accidents (CVA, p = 0.03) vs. controls, more pronounced in higher severity variants. 5'UTR variants were associated with an increased risk of diabetes (p < 0.001) and a younger age at diabetes diagnosis (p = 0.003) compared to other variants. In multivariable analysis, 5'UTR variants were associated with an increased risk of diabetes (odds ratio 2.97, 95% confidence interval 1.78-4.80, p < 0.001). Increasing reticulocyte levels positively correlated with metabolic syndrome markers (serum glucose, glycated hemoglobin, and triglyceride levels) and mediated the increased diabetes risk of 5'UTR variant carriers.</p><p><strong>Conclusions: </strong>VHL gene variant carriers have an increased risk of diabetes and CVA. Mediation analysis suggests pseudohypoxia as a possible mechanism.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"239"},"PeriodicalIF":8.5,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SREBP1 deficiency aggravates vascular calcification via iASPP-triggered ferroptosis of vascular smooth muscle cells.","authors":"Yunhui Wu, Binhong Yang, Haoqi Sun, Meijuan Cheng, Jingjing Jin, Dongxue Zhang, Lixin Chang, Shenglei Zhang, Yaling Bai, Jinsheng Xu","doi":"10.1186/s12933-025-02797-3","DOIUrl":"10.1186/s12933-025-02797-3","url":null,"abstract":"<p><strong>Background: </strong>Vascular calcification (VC) is frequently observed in patients with chronic kidney disease (CKD), which seriously affects the structure and function of blood vessels. Ferroptosis, a type of cell death caused by iron-catalyzed reactive oxygen species (ROS) and lipid peroxidation, has been implicated in cardiovascular diseases, including VC. However, the underlying molecular mechanisms of ferroptosis in VSMCs remain poorly understood.</p><p><strong>Methods: </strong>Bioinformatics analysis was employed to mine the dataset and screen sterol regulatory element-binding protein 1 (SREBP1) related to ferroptosis and VC. Quantitative real-time polymerase chain reaction, western blotting, immunofluorescence, and immunohistochemistry were used to analyze gene expression. Functional experiments were conducted to comprehensively investigate the effects of SREBP1 on ferroptosis and VC. Chromatin immunoprecipitation (ChIP) analysis and dual-luciferase reporter assays were utilized to further elucidate the regulatory effects of SREBP1 on the inhibitor of apoptosis-stimulating protein of p53 (iASPP).</p><p><strong>Results: </strong>We identified that liproxstatin-1 (Lip-1), as a ferroptosis-specific inhibitor, dose-dependently impeded calcification progression, highlighting the pivotal roles of lipid peroxidation. Furthermore, we obtained clues that SREBP1, a lipid-regulating transcription factor, was associated with calcification and ferroptosis by investigating the GEO and FerrDB databases. Subsequently, we observed that SREBP1 was significantly downregulated in serum and calcified radial arteries of CKD patients, in calcified aortas from CKD mice, and in calcified VSMCs. The low SREBP1 expression was inversely correlated with ferroptosis in vivo and in vitro, respectively. Overexpression of SREBP1 remarkably attenuated osteogenic differentiation and calcium deposition of VSMCs by suppressing ferroptosis. Mechanistically, we demonstrated that SREBP1 bound to the promoter region of iASPP and directly promoted the expression of iASPP. Moreover, iASPP silencing exacerbated ferroptosis and calcification of VSMCs. Rescue experiments revealed that SREBP1 exerted the protective effects on VC that were achieved in part by regulating the activation of iASPP. In vivo experiments further elucidated that artery-specific SREBP1 overexpression alleviated ferroptosis and calcification via the SREBP1/iASPP axis in CKD mice.</p><p><strong>Conclusions: </strong>These findings report that targeting SREBP1 or iASPP may represent an attractive interventional strategy for VC in CKD.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"236"},"PeriodicalIF":8.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12135566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Statin-induced risk of diabetes does not reduce cardiovascular benefits in primary prevention: a 6-year propensity-score matched study in a large population.","authors":"Maria Lembo, Valentina Trimarco, Raffaele Izzo, Daniela Pacella, Stanislovas S Jankauskas, Paola Gallo, Roberto Piccinocchi, Carmine Morisco, Gaetano Piccinocchi, Luca Bardi, Stefano Cristiano, Giovanni Esposito, Giuseppe Giugliano, Fahimeh Varzideh, Maria Virginia Manzi, Bruno Trimarco, Gaetano Santulli","doi":"10.1186/s12933-025-02798-2","DOIUrl":"10.1186/s12933-025-02798-2","url":null,"abstract":"<p><strong>Background: </strong>The long-term risk of cardiovascular (CV) events in individuals who develop new-onset type 2 diabetes (T2D) after having received statin therapy in primary prevention is mostly unknown.</p><p><strong>Methods: </strong>We designed a population-based cohort study in individuals without T2D and atherosclerotic CV disease (ASCVD), divided in two groups according to the presence or not of statin therapy. We also balanced the study groups for demographic and clinical factors using propensity score matching.</p><p><strong>Results: </strong>119307 individuals without T2D and ASCVD were divided in statin users (N = 90906) or not (N = 28401) and followed-up for 70.1 ± 61.3 months. Yearly incidence of T2D rate was 0.3% in the control group and 2.2% in the statin treated group. A Cox regression analysis confirmed the association between incident T2D and statin therapy. In normotensive individuals, the presence of statin therapy led to a 2-fold risk to develop incident T2D with a HR 2.61 (95% CI 2.11-3.22, p < 0.001) which was also that of statin untreated hypertensive patients. In the hypertensive population statin therapy was associated with a HR of incident T2D of 4.62 (95% CI 3.75-5.69, p < 0.001). CV events rate, including coronary and cerebrovascular fatal and non-fatal events, was 1.9% in the statin group vs. 0.7% in the control group and a multiple regression analysis demonstrated an association between statin therapy and CV events. A further Cox regression performed only in the statin treated population revealed a significant association of CV events with age, serum creatinine levels, and incident T2D. Of note, the increased rate of new-onset T2D associated with statin use does not modify the class of CV risk of this population. All these findings were confirmed at the propensity score matched analysis.</p><p><strong>Conclusions: </strong>Statin therapy in primary prevention is associated with a higher risk of incident T2D, especially in hypertensive patients. However, since the final CV risk of those who develop T2D during statin treatment was lower than the one required for statin prescription according to the ESC guidelines, indicating that this phenomenon does not impair the benefit in CV prevention associated with the lipid lowering effect of statins.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"233"},"PeriodicalIF":8.5,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tenascin-C drives cardiovascular dysfunction in a mouse model of diabetic cardiomyopathy.","authors":"Zsuzsanna Arnold, Christopher Dostal, Petra Lujza Szabó, Ibrahim Aykac, Ana Isabel Antunes Goncalves, Silva Laura Sousa, Simge Baydar, Heidi Budde, Barnabás Váradi, György L Nadasy, Mária Szekeres, Camilla Hage, Lars H Lund, Sarah Costantino, Dietmar Abraham, Karin Zins, Seth Hallström, Martin Bilban, Bence Ágg, Nazha Hamdani, Péter Ferdinandy, Francesco Paneni, Attila Kiss, Bruno K Podesser","doi":"10.1186/s12933-025-02780-y","DOIUrl":"10.1186/s12933-025-02780-y","url":null,"abstract":"<p><strong>Background: </strong>Diabetic cardiomyopathy (DCM) is a complex condition linked to diabetes, characterized by cardiac and vascular dysfunction, frequently concomitant with heart failure with preserved ejection fraction. The extracellular matrix glycoprotein Tenascin-C (TNC) has been found to be upregulated under diabetic conditions. However, the potential contributory role of TNC in the progression of DCM remains largely unclear. This study was designed to elucidate the role of TNC in the pathogenesis of DCM.</p><p><strong>Methods: </strong>Diabetes was induced in adult male wild-type (WT) and TNC knockout (TNC-KO) mice, through the administration of streptozotocin (50 mg/kg) for five consecutive days. At 18 weeks cardiac and aortic vascular function was evaluated using echocardiography and wire myography. Myocardium and plasma samples were collected for biochemical, histological, and molecular analyses. Cardiomyocytes and cardiac fibroblasts were used to investigate the impact of diabetes on TNC expression, inflammation, myocardial stiffness and function. Additionally, transcriptomic analysis of cardiac tissue by RNA-sequencing was conducted. Plasma TNC levels were assessed by enzyme-linked immunosorbent assay in cohorts of heart failure patients and type 2 diabetes mellitus.</p><p><strong>Results: </strong>TNC-KO diabetic mice showed preserved left ventricular systolic and diastolic function, significantly reduced cardiac fibrosis and mitigated endothelial dysfunction compared to WT diabetic animals. Compared with cardiomyocytes of diabetic WT animals, cardiomyocytes of TNC-KO mice developed less stiffness (Fpassive). Additionally, exposing mouse cardiomyocytes and human cardiac fibroblasts to high glucose stress (30 mM) led to a significant increase in TNC expression. Conversely, recombinant human TNC promoted pro-inflammatory and oxidative stress markers in cardiomyocytes. The role of TNC in fibrosis and DCM was found to involve pathways related to p53 signaling and Serpin1k, Ccn1, Cpt1a, and Slc27a1, as identified by RNA sequencing analysis. Additionally, plasma TNC levels were significantly elevated in patients with heart failure, irrespective of diabetes status, compared to healthy individuals.</p><p><strong>Conclusions: </strong>Our findings indicate that in diabetes, TNC contributes to cardiac contractile dysfunction, myocardial fibrosis, oxidative stress, inflammation, and metabolic disturbances in diabetic mouse heart. These results implicate the potential of TNC inhibition as a novel therapeutic approach for treating DCM.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"235"},"PeriodicalIF":8.5,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of dietary interventions on cardiometabolic health.","authors":"Erind Gjermeni, Raluca Fiebiger, Linnaeus Bundalian, Antje Garten, Torsten Schöneberg, Diana Le Duc, Matthias Blüher","doi":"10.1186/s12933-025-02766-w","DOIUrl":"10.1186/s12933-025-02766-w","url":null,"abstract":"<p><p>Obesity and cardiometabolic diseases are leading causes of morbidity and mortality among adults worldwide. These conditions significantly contribute to and exacerbate other major causes of illness and death, including cancer, neurodegenerative diseases, and chronic kidney disease. The growing burden of these diseases has increased the interest of modern medicine in understanding metabolic processes and health, with diet emerging as a pivotal modifiable factor, alongside physical inactivity and smoking. In this review, we discuss the pathophysiological and evolutionary foundations of metabolic processes that may link \"unhealthy\" nutrition to obesity and cardiometabolic diseases and review the current literature to assess the effects of various diet interventions and patterns on cardiometabolic parameters. Special emphasis is placed on summarizing the latest, albeit partially contradictory, evidence to offer balanced dietary recommendations with the ultimate aim to improve cardiometabolic health.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"234"},"PeriodicalIF":8.5,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of dapagliflozin on the progression of left ventricular dysfunction in type 2 diabetes mellitus: a randomized controlled trial.","authors":"Thomas H Marwick, Amera Halabi, Cheng Hwee Soh, Annie Curtin, Ashleigh-Georgia Sherrif, Atro Azad, Leah Wright","doi":"10.1186/s12933-025-02796-4","DOIUrl":"10.1186/s12933-025-02796-4","url":null,"abstract":"","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"232"},"PeriodicalIF":8.5,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased prevalence and risk of atherosclerotic cardiovascular disease in individuals with Type 1 diabetes and metabolic dysfunction-associated steatotic liver disease.","authors":"Jonathan Mertens, Jonas Weyler, Eveline Dirinck, Luisa Vonghia, Wilhelmus J Kwanten, Luc F Van Gaal, Benedicte Y De Winter, Sven Francque, Christophe De Block","doi":"10.1186/s12933-025-02764-y","DOIUrl":"10.1186/s12933-025-02764-y","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the correlation between metabolic dysfunction-associated steatotic liver disease (MASLD) and atherosclerotic cardiovascular disease (ASCVD) in individuals with type 1 diabetes (T1D).</p><p><strong>Methods: </strong>Adults with T1D (n = 659) were consecutively screened for liver steatosis via abdominal ultrasound. The presence of macrovascular disease (including coronary artery disease [CAD], peripheral artery disease [PAD], or ischaemic stroke [CVA, cerebrovascular accident]) was identified via electronic medical records. The 5- and 10-year risks of fatal/nonfatal ASCVD were assessed via the Steno Type 1 Risk Engine. Insulin resistance was assessed via the estimated glucose disposal rate (eGDR).</p><p><strong>Results: </strong>The MASLD prevalence was 16.8%. The prevalence of composite ASCVD (18.9 vs. 6.8%, p < 0.001), CAD (9.9 vs. 4.7%, p = 0.031), PAD (9.0 vs. 2.2%, p < 0.001) and CVA (6.3 vs. 1.1%, p = 0.002) was greater in people with MASLD. The 5-year (7.8 [2.1-14.4] vs. 4.8 [1.6-12.0]%, p = 0.034) and 10-year (15.0 [4.1-26.8] vs. 9.4 [3.1-22.5]%, p = 0.035) risks of ASCVD were greater in those with MASLD. MASLD was associated with prevalent ASCVD (adjusted OR 4.26, 95% CI 1.79-10.11, p < 0.001), independent of age, sex, diabetes duration, smoking, statin use, LDL-cholesterol, the glomerular filtration rate, albuminuria, and metabolic syndrome.</p><p><strong>Conclusion: </strong>MASLD is associated with both an increased prevalence of ASCVD and an increased calculated risk of fatal/nonfatal ASCVD in people with T1D.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"24 1","pages":"230"},"PeriodicalIF":8.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}