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The gut microbiota is one of the key elements responsible for maintaining the body’s homeostasis. Its diverse composition affects, among others, the digestive and immune systems and also the circulatory system. Imbalances within the microbial community, referred to as dysbiosis, may lead to increased intestinal barrier permeability, chronic inflammation, and abnormal immune responses, which can be associated with the development of numerous diseases. Gut dysbiosis results in disturbances in the production of short-chain fatty acids, which exert anti-inflammatory effects, regulate blood pressure, and inhibit cardiac fibrosis. At the same time, it promotes the increased synthesis of trimethylamine N-oxide, a metabolite linked to inflammation, endothelial dysfunction, a higher risk of thrombosis, and the occurrence of arrhythmias. Additionally, small intestinal bacterial overgrowth (SIBO) may increase inflammation and contribute to metabolic and cardiovascular diseases (CVDs). The gut microbiota also influences the immune system through the production of neurotransmitters and modulation of T-cell activity, which may play a role in the development of autoimmune diseases. Reduced microbial diversity and an increased abundance of pathogenic bacteria are observed in individuals with hypertension and CVD, underscoring the importance of the microbiota as both a preventive and therapeutic factor. These findings highlight the crucial role of the gut microbiota in maintaining cardiovascular health and emphasize the need for further research into its modulation in the treatment of chronic diseases. Full article

Cardiovascular disease (CVD) continues to be the primary cause of morbidity and mortality worldwide, underscoring the urgent need for novel therapeutic alternatives. In recent years, marine ecosystems have garnered increasing attention as a promising source of bioactive compounds with unique structural and pharmacological properties. Marine-derived toxins and venoms, including tetrodotoxin, ω-conotoxins, anthopleurins, palytoxin, brevetoxin, aplysiatoxin, and asterosaponins, exert cardioprotective effects through diverse mechanisms such as modulation of ion channels, inhibition of sympathetic overactivity, antioxidative actions, and enhancement of myocardial contractility. These properties make them potential candidates for addressing various CVD manifestations, including arrhythmia, hypertension, ischemia–reperfusion injury, and heart failure. However, despite their therapeutic promise, the clinical application of these marine compounds remains limited due to poor tissue selectivity, narrow therapeutic indices, proinflammatory activity, and limited metabolic stability. Structural modifications, advanced drug delivery platforms, and in vivo validation studies are crucial for overcoming these challenges. This review highlights the pharmacological actions, molecular targets, and cardiovascular relevance of selected marine toxins and venoms while also addressing key translational barriers. Advances in biotechnology and peptide engineering are enabling the safer and more targeted use of these compounds. Collectively, marine-derived toxins and venoms represent a largely untapped but highly promising frontier in cardiovascular drug discovery. Strategic research focused on elucidating mechanisms, optimizing delivery, and translating clinical applications will be critical to unlocking their full therapeutic potential. Full article

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide. CVDs are associated with multiple factors, including oxidative stress, mediated endothelial dysfunction, vascular inflammation, and atherothrombosis. Although traditional antioxidant supplementation (such as vitamins C, E, and β-carotene) has shown promising results in rigorous animal model studies, it has consistently failed to demonstrate clinical benefit in most human trials. Consequently, there is a substantial unmet need for novel paradigms involving mechanistically and biologically relevant pharmaceutical-grade antioxidant therapies (“next-generation antioxidants”). Rapid advancements in redox biology, nanotechnology, genetic modulation of redox processes, and metabolic regulation have enabled the development of new antioxidant therapeutics, including mitochondrial-targeted agents, NADPH oxidase (NOX) inhibitors, selenoprotein and Nrf2 activators, engineered nanoparticles, catalytic antioxidants, and RNA-based and gene-editing strategies. These interventions have the potential to modulate specific oxidative pathways that contribute to CVD pathogenesis. This review provides a comprehensive assessment of current oxidative stress–modulating modalities and their potential to inform personalized cardiovascular prevention and treatment strategies. Full article

Cardiovascular disease (CVD) is increasingly recognized as a significant comorbidity in people living with HIV (PWH), contributing to increased morbidity and mortality. Epidemiological studies indicate that PWH have a 1.2–2-fold higher risk of myocardial infarction (MI) and other CVD events compared to HIV-negative individuals. While the mechanisms underlying HIV-associated CVD are not fully understood, they are likely to include a combination of cardiovascular-related adverse effects of HIV medications, vascular dysfunction caused by HIV-induced monocyte activation, and cytokine secretion, in addition to existing comorbidities and lifestyle choices. This comprehensive review examines the complex relationship between HIV infection and CVD, highlighting key pathophysiological mechanisms such as chronic immune activation, inflammation, endothelial dysfunction, and the role of antiretroviral therapy (ART) in promoting cardiovascular risk. Alongside conventional risk factors such as smoking, hypertension, and dyslipidemia, HIV-specific elements, especially metabolic abnormalities associated with ART, significantly contribute to the development of CVD. Prevention strategies are crucial, focusing on the early identification and management of cardiovascular risk factors as well as optimizing ART regimens to minimize adverse metabolic effects. Clinical guidelines now recommend routine cardiovascular risk assessment in PWH, emphasizing aggressive management tailored to their unique health profiles. However, challenges exist in fully understanding the cardiovascular outcomes in this population. Future research directions include exploring the role of inflammation-modulating therapies and refining sustainable prevention strategies to mitigate the growing burden of CVD in PWH. Full article

The natural polypeptide drug hirudin, a direct thrombin inhibitor, exhibits potent anticoagulant, anti-myocardial fibrotic, and anti-inflammatory effects in the treatment of cardiovascular diseases (CVD), but its clinical application remains limited by its low bioavailability, insufficient targeting capability, and bleeding risk. In recent years, the development of nanotechnology has enabled peptide drug delivery systems to demonstrate substantial promise in medical practice. Significant progress has been made in overcoming limitations and enhancing therapeutic efficacy against CVD through the use of Hirudin-based drug delivery systems by addressing drug stability in vivo, improving targeting ability, and ultimately achieving responsive release. This paper systematically reviews the mechanisms of action, clinical applications, and novel delivery strategies of the peptide drug hirudin in the treatment of CVD, with a particular focus on recent advances in hirudin-based drug delivery systems, and it also looks forward to future research directions for hirudin delivery systems, including the development of scalable intelligent carriers, the construction of real-time feedback systems, and the establishment of standardized in vitro and in vivo evaluation systems, aiming to present novel strategies for safe and efficient treatment of CVD. Full article

This study aimed to identify metabolomic biomarkers for diabetes progression and validate their response to lifestyle intervention. A two-phase design was employed: first, untargeted metabolomics distinguished normoglycemic, prediabetic (PDM), and diabetic (DM) individuals, identifying 1,5-anhydroglucitol (1,5-AG) as the most significant biomarker for differentiating PDM from DM (apparent AUC = 0.97, 95% CI: 0.95–1.00; corrected AUC = 0.94, 95% CI: 0.83–1.00; q < 0.001). Second, in a 3-month randomized controlled trial involving 300 adults with PDM, the combined diet and exercise intervention significantly improved fasting blood glucose and glycated hemoglobin levels, while concurrently elevating serum 1,5-AG levels compared with the control group, though it did not yield significant improvements in other cardiovascular disease-related risk factors including body mass index, waist circumference, systolic blood pressure, and diastolic blood pressure. The intervention also showed a trend toward reduced diabetes incidence. Integrated analysis establishes 1,5-AG as a sensitive biomarker of dysglycemia that is responsive to lifestyle modification, supporting its potential as a mechanistic tool for monitoring intervention efficacy in diabetes prevention. Full article

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and constitute a substantial economic burden. Despite population aging, recent years have witnessed an increasing prevalence of conditions such as heart failure (HF), including among young adults. In this context, coronary artery disease (CAD) has also become an increasingly discussed issue. It has long been recognized that control of risk factors is crucial for prevention. Researchers stress the need to monitor these factors from the earliest stages of life, and detailed analyses indicate an influence of the prenatal period on the development of chronic diseases, including cardiovascular disorders. Transgenerational and intergenerational epigenetic mechanisms are also taken into account. This review aims to systematically evaluate the existing literature and summarize the mechanisms that may link these factors. We consider epigenetic, metabolic, immunological, and inflammatory influences. We describe examples of environmental exposures, such as air pollution, maternal diet, toxins, and infections, and analyze data derived from clinical studies. We discuss gaps in the literature and identify limitations, outlining directions for future research and emphasizing the need for CVD prevention initiated at the earliest stages of life. Full article

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. This increases the demand for real-world evidence to complement findings from randomized controlled trials. The German IQVIA Disease Analyzer (DA) database, which is populated with anonymized electronic medical records from general practitioners and specialists, has become an increasingly valuable source for cardiovascular research. Over the past two decades, and especially between 2020 and 2025, numerous epidemiological studies have used this database to explore associations between cardiovascular risk factors, comorbidities, therapeutic patterns, and cardiovascular outcomes in large, broadly representative outpatient populations. This review synthesizes evidence from 13 selected DA-based studies examining atrial fibrillation, heart failure, cardiometabolic disease, lipid management, non-alcoholic fatty liver disease (NAFLD)–related cardiovascular risks, cerebrovascular complications, COVID-19-associated vascular events, and modifiable behavioral and anthropometric factors. These studies were selected based on predefined criteria including cardiovascular relevance, methodological rigor, large sample size, and representativeness of key disease domains across the 2000–2025 period. Eligible studies were identified through targeted searches of peer-reviewed literature using the German IQVIA Disease Analyzer database and were selected to reflect major cardiovascular disease domains, risk factors, and therapeutic areas. Across disease domains, the reviewed studies consistently demonstrate the DA database’s capacity to identify reproducible associations between cardiometabolic risk factors, comorbidities, and cardiovascular outcomes in routine outpatient care. While causal inference is not possible, the database enables the identification of clinically meaningful associations that inform hypothesis generation, help quantify disease burden, and highlight gaps in prevention or treatment. The database’s strengths include large sample sizes (often exceeding 100,000 patients), long follow-up periods, and high external validity, while limitations relate to coding accuracy, residual confounding, and the absence of detailed clinical measures. Collectively, the evidence underscores the importance of the DA database as a crucial platform for real-world cardiovascular research. Full article

The quality of high-density lipoproteins (HDLs) is characterized by lipid and protein composition, oxidation and glycation extent, and particle size, while the quantity of HDL-C is just the cholesterol amount in HDL. The inverse association between HDL-C and cardiovascular disease (CVD) and hypertension has been well established; however, the U-shaped mortality risk observed from HDL-C underscores that HDL quality and function are equally important. The present cross-sectional study assessed the correlations of serum lipid and glucose profiles, and low-density lipoprotein (LDL) and HDL characteristics, with blood pressure (BP) distribution in ordinary middle-aged Korean participants (n = 50; mean age 47.0 ± 11.7 years; males: n = 25, 49.2.0 ± 11.7 years; females: n = 25, 44.8 ± 11.5 years), with particular focus on HDL quality and its antioxidant capacity. This study observed that serum elevated triglyceride (TG) and glucose levels were directly proportional to elevated systolic BP (SBP) and diastolic BP (DBP), whereas serum total cholesterol (TC), LDL-C, and HDL-C were not correlated with BP. However, HDL-C/TC (%) was negatively associated with SBP (p = 0.036), while TG/HDL-C and glucose/HDL-C ratios were positively associated with both SBP and DBP, suggesting that TG and glucose proportions relative to HDL-C are probable predictors of hypertension. Elevations of TG, oxidation, and glycation in LDL were positively associated with elevations of BP, whereas LDL particle size was negatively correlated with BP. Similarly, elevations of TG and glycation in HDL₂ and HDL₃ were positively correlated with elevations of BP, while the particle size of HDL₂ was negatively correlated with BP. The heightened HDL₂-associated paraoxonase (PON) activity and ferric ion reduction ability (FRA) negatively correlated with LDL oxidation and particle size, whereas elevated HDL₃-associated PON and FRA activities were inversely related to LDL glycation. An enhanced glycation in HDL₂ was negatively correlated with HDL₂-associated PON activity and FRA, while an increase in HDL₂ particle size was only dependent on the associated PON activity but not on FRA. In conclusion, observational outcomes demonstrated that improved HDL quality and functionality (characterized by large particle size, reduced glycation, and higher FRA and PON activities) were inversely correlated with LDL oxidation, glycation, particle shrinkage, and the risk of hypertension. Full article

Background: Childhood obesity represents the most common nutritional and metabolic disorder in industrialized countries and constitutes a major public health concern. In Italy, 20–25% of school-aged children are overweight and 10–14% are obese, with marked regional variability. Excess adiposity in childhood is frequently associated with hypertension, dyslipidemia, insulin resistance, and non-alcoholic fatty liver disease (NAFLD), predisposing to future cardiovascular disease (CVD). Objective: To investigate anthropometric indicators of cardiometabolic risk in 810 children and adolescents aged 7–17 years who underwent assessment for competitive sports eligibility at the Sports Medicine Unit of Modena, evaluate baseline knowledge of cardiovascular health aligned with ESC, AAP (2023), and EASO guidelines. Methods: 810 children and adolescents aged 7–17 years undergoing competitive sports eligibility assessment at the Sports Medicine Unit of Modena underwent evaluation of BMI percentile, waist circumference (WC), waist-to-height ratio (WHtR), and blood pressure. Cardiovascular knowledge and lifestyle habits were assessed via a previously used questionnaire. Anthropometric parameters, blood pressure (BP), and lifestyle-related knowledge and behaviors were assessed using standardized procedures. Overweight and obesity were defined according to WHO BMI-for-age percentiles. Elevated BP was classified based on the 2017 American Academy of Pediatrics age-, sex-, and height-specific percentiles. Statistical analyses included descriptive statistics, group comparisons, chi-square tests with effect size estimation, correlation analyses, and multivariable logistic regression models. Results: Overall, 22% of participants were overweight and 14% obese. WHtR > 0.5 was observed in 28% of the sample and was more frequent among overweight/obese children (p < 0.001). Elevated BP was detected in 12% of participants with available measurements (n = 769) and was significantly associated with excess adiposity (χ² = 7.21, p < 0.01; Cramér’s V = 0.27). In multivariable logistic regression analyses adjusted for age and sex, WHtR > 0.5 (OR 2.14, 95% CI 1.32–3.47, p = 0.002) and higher sedentary time (OR 1.41 per additional daily hour, 95% CI 1.10–1.82, p = 0.006) were independently associated with elevated BP, whereas BMI percentile lost significance when WHtR was included in the model. Lifestyle knowledge scores were significantly lower among overweight and obese participants compared with normal-weight peers (p < 0.01). Conclusions: WHtR is a sensitive early marker of cardiometabolic risk, often identifying at-risk children missed by BMI alone. Baseline cardiovascular knowledge was suboptimal. The observed gaps in cardiovascular knowledge underscore the importance of integrating anthropometric screening with structured educational interventions to promote healthy lifestyles and long-term cardiovascular prevention. Full article

Non-communicable diseases, particularly cardiovascular diseases (CVD) and metabolic syndrome (MS), remain a major challenge for primary health care (PHC). This study aimed to assess cardiometabolic risk and health behaviours in adult PHC patients using routine preventive screening. This prospective observational study included 506 adults attending routine consultations in an urban PHC centre in Poland. Preventive assessment included anthropometric measurements (body weight, height, BMI, and waist circumference), blood pressure, lipid profile, and fasting glucose levels. Health behaviours were recorded using the standardised NFZ CHUK questionnaire. The 10-year CVD risk was estimated using the SCORE2 algorithm. Multivariable logistic regression was used to identify independent factors associated with high cardiovascular risk (SCORE2 ≥ 5%) and of a composite endpoint defined as the presence of any non-optimal biochemical parameter. Nearly half of the participants had excess body weight (overweight or obesity), and more than half met criteria for central obesity. Borderline or elevated total cholesterol was found in 47% of patients, abnormal LDL in 27%, low HDL-C (<40 mg/dL) in 80% (84% when applying sex-specific cut-offs), and impaired fasting glucose or diabetes in about 12%. High SCORE2 risk (≥5%) was observed in approximately 9% of the cohort. In multivariable models, SCORE2 components (age, sex, and smoking) were, as expected, associated with high SCORE2 risk, and obesity (BMI ≥ 30 kg/m²)—a factor not included in SCORE2—was additionally associated with higher risk. Additionally, age, male sex, and obesity also predicted the presence of at least one non-optimal biochemical marker. The prevalence of high SCORE2 risk increased from 1.2% in patients with 0–1 modifiable risk factor to 25.7% in those with 4–5 factors. Lower educational attainment was associated with a higher proportion of high-risk individuals in univariate analysis. Routine preventive activities in PHC enable the identification of important lipid and glucose abnormalities and the clustering of modifiable risk factors, even in a relatively young, highly educated population. Systematic cardiovascular screening and a focus on patients with accumulated risk factors should remain a priority in PHC to enable early identification of high-risk patients and timely implementation of lifestyle and therapeutic interventions. Full article

Cardiovascular disease (CVD) remains a leading cause of global morbidity and mortality, and its initiation and progression are closely associated with multiple molecular mechanisms. Neutrophil extracellular traps (NETs) are mesh-like structures composed of DNA, histones, and antimicrobial proteins that are released by neutrophils during inflammation or infection. They play a crucial role in innate immune defense. However, when the dynamic balance of NETs is disrupted by excessive formation, persistent accumulation, or impaired clearance, NETs are no longer merely bystanders. Instead, they actively drive pathological processes in multiple CVDs and serve as a critical link between inflammation and cardiovascular injury. Given the central role of NETs in CVD pathogenesis, including atherosclerosis, myocardial ischemia–reperfusion injury, pulmonary arterial hypertension, atrial fibrillation, and heart failure, therapeutic strategies targeting NETs, such as inhibiting aberrant formation, enhancing clearance, or neutralizing toxic components, have emerged as promising approaches. In recent years, traditional Chinese medicine (TCM) and natural products have shown potential therapeutic value by modulating NET formation and promoting NET degradation, owing to their multitarget, multipathway regulatory effects. This article reviews the mechanisms by which NETs operate in CVDs and explores potential pathways through which TCM and natural active ingredients prevent and treat CVDs by regulating NETs. This review provides theoretical support for further research and clinical application. Full article

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide, with growing evidence indicating that epigenetic mechanisms play a central role in their onset and progression. This review provides a comprehensive overview of current knowledge on the epigenetic regulation and molecular mechanisms involved in CVDs, as well as their potential therapeutic implications. The findings demonstrate that DNA methylation, histone modifications, and non-coding RNAs are key regulators of gene expression associated with cardiac hypertrophy, atherosclerosis, myocardial infarction, and heart failure. Interactions between epigenetic alterations and inflammatory or oxidative stress pathways further contribute to endothelial dysfunction and vascular remodeling. Emerging therapeutic strategies targeting these mechanisms, including histone deacetylase inhibitors, DNA methyltransferase inhibitors, and RNA-based therapeutics, show promising cardioprotective effects in experimental and early clinical studies. Overall, this review underscores the significance of epigenetic regulation in cardiovascular pathophysiology and highlights the potential of epigenetic-based interventions as a foundation for precision medicine and novel therapeutic approaches in cardiology. Full article

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality, despite advances in pharmacological prevention and treatment. The burden of CVD necessitates implementing the treatment of risk factors including dyslipidemia. Pharmaceutical advancements and in depth understanding of pathophysiology have enabled innovative therapies targeting pathways underlying lipoprotein metabolism disorders. Angiopoietin protein-like 3 (ANGPTL3) plays a crucial role in the regulation of lipoprotein metabolism, therefore being a potential therapeutic target. Inhibition of ANGPTL3 has emerged as a new therapeutic strategy to reduce LDL-cholesterol levels independent of the LDL receptor function. Therapeutic approaches for ANGPTL3 inhibition range from monoclonal antibodies to nucleic acid therapeutics including antisense oligonucleotides and small interfering RNAs. In this review, we briefly explain the structure and mechanism of action of ANGPTL3 and discuss the therapeutic approaches for targeting ANGPTL3 in the clinical setting. We also discuss Evinacumab, a monoclonal antibody, its structure, mechanism of action, safety, tolerability, pharmacokinetics, and pharmacodynamics, as well as its clinical trial-derived results. The antisense oligonucleotides modify ANGPTL3 mRNA to inhibit protein production, and small interfering RNAs induce mRNA degradation; results from clinical trials were reviewed in detail. Finally, we discuss promising gene editing approaches including clustered regularly interspaced short palindromic repeats (CRISPR)/Cas systems. Full article

Prediabetes is a serious and major global problem afflicting approximately 21% of the world’s population. It is the intermediate stage between normal glucose levels and type 2 diabetes mellitus (T2DM). Prediabetes is associated with major complications including the development of T2DM and increased cardiovascular disease (CVD). It can be easily diagnosed with an inexpensive plasma glucose level and/or a hemoglobin A1c (HbA1c) measurement. The mainstay of treatment is intensive lifestyle (ILS) intervention, including reduction in calories, especially saturated fats, refined carbohydrates, etc., coupled with regular physical activity of 150 min per week since ILS changes, with at least a 5% weight loss, have been shown to reduce progression to T2DM in multiple studies globally. Also, metformin therapy has been shown to prevent the progression to T2DM. In conclusion, serious consideration by guideline committees to classify prediabetes as a disease is highly recommended based on its global burden, easy and cost-effective diagnosis, association with serious conditions of diabetes and CVD, and effective ILS intervention. Therapy targeting those at an especially high risk for T2DM, such as persons with impaired glucose tolerance (IGT), impaired fasting glucose (IFG) with values ≥ 110 mg/dL (6.1 mmol/L), and/or HbA1c ≥ 6.0% (42 mmol/mol) coupled with overweightness or obesity. Full article