Cardiovascular diseases remain the leading cause of global morbidity and mortality, imposing a significant burden on families and societies. E26 transformation‑specific (ETS)‑1 and ETS‑2, members of the ETS family of transcription factors (also known as proto‑oncogenes), are increasingly recognized for their roles in tumor progression. Recent studies highlight their importance in normal coronary artery development, myocardial homeostasis and the regulation of vascular inflammation and remodeling. Emerging evidence suggests that ETS‑1/ETS‑2 are critical in the pathogenesis of atherosclerosis, myocardial ischemia‑reperfusion injury, cardiac remodeling and heart failure. The present review summarized the research progress of ETS‑1/ETS‑2 in cardiovascular diseases, discusses the relevant challenges encountered in the translational process of ETS‑1/ETS‑2‑targeted therapy for cardiovascular diseases and provides novel strategies for the treatment of cardiovascular diseases targeting ETS‑1/ETS‑2.

This narrative review examines the nutritional composition, bioactive compounds, and mechanistic pathways of red beetroot (Beta vulgaris L.), as well as its health effects. Beetroot, obtained from the red beet (Beta vulgaris) plant, is now receiving considerable attention thanks to its high levels of nitrates, betalains, polyphenols, and antioxidants. Its rich contents of bioactive compounds have recently led to its recognition as a "superfood." This root vegetable contains phytochemicals, including betacyanins and betaxanthins; dietary nitrates; and various phenolic compounds that contribute to its distinctive color and health-promoting properties. Red beets are noted for their beneficial effects in the management of cardiovascular, metabolic, inflammatory, and gastrointestinal diseases, as well as hyperglycemia and dyslipidemia. They also exhibit antioxidant, anti-inflammatory, anticarcinogenic, antiatherogenic, antidiabetic, and neuroprotective properties. Furthermore, they play supportive roles in managing diseases such as metabolic syndrome by reducing inflammation and oxidative stress. They also contribute to health by preventing cellular damage caused by free radicals, strengthening the immune system, and promoting cell regeneration. While the health benefits of beetroot are supported by in vivo, in vitro, and human studies, further research is needed to determine its long-term effects on metabolic diseases. This review examines the chemical composition, nutritional elements, and bioactive compounds of beetroot, synthesizing information about their molecular and cellular mechanisms of action and their effects on human health as evidenced by clinical studies. Recommendations for future research are also provided. Mechanistic evidence from preclinical models is discussed separately from findings derived from human clinical trials.

Dementia encompasses distinct subtypes characterized by different underlying mechanisms-most notably, Alzheimer's disease (AD), driven by neurodegeneration, and vascular dementia (VaD), stemming from cerebrovascular pathology. Growing evidence emphasizes the critical role of neuroinflammatory processes in both conditions, highlighting inflammatory biomarkers as potential tools for differential diagnosis. This study assesses the diagnostic accuracy of inflammatory biomarkers in distinguishing AD from VaD.

A systematic search of PubMed, EMBASE, Web of Science, and Cochrane Library databases was conducted in November 2025 to identify eligible studies. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated to compare inflammatory marker levels between AD and VaD groups. Random-effects models were applied for all meta-analyses.

Fifteen observational studies involving 1728 participants were included. Pooled analyses showed no significant differences in IL-6 (SMD: -0.13; 95% CI: -0.44 to 0.19; p = 0.433), TNF-α (SMD: -0.22; 95% CI: -0.71 to 0.28; p = 0.388), or CRP (SMD: 0.73; 95% CI: -0.17 to 1.62; p = 0.111) between AD and VaD overall. However, subgroup analyses indicated context-dependent variations: IL-6 and TNF-α levels were lower in patients with AD in studies conducted in Eastern regions, with larger sample sizes (≥100 participants), older populations (≥70 years), or higher methodological quality. CRP showed similar patterns in larger or higher-quality studies. Importantly, IL-1β levels were significantly higher in patients with AD compared to patients with VaD (SMD: 0.48; 95% CI: 0.18 to 0.79; p = 0.002).

Exploratory analyses suggest IL-1β as a promising candidate for differentiating AD from VaD, warranting validation in larger, prospective studies. The preliminary, context-dependent signals for IL-1β, IL-6, and TNF-α indicate that inflammatory pathways differ between these dementias but are substantially influenced by methodological and population factors.

 INPLASY platform (number: INPLASY202570068).

Tolvaptan is widely used as an adjunct oral diuretic to loop and thiazide diuretics for the management of fluid overload in patients with congestive heart failure. Recently, tolvaptan sodium phosphate (TSP), a water-soluble prodrug of tolvaptan, was developed for intravenous administration and has demonstrated efficacy and safety in clinical settings. However, cases of TSP ineffectiveness have not yet been reported. Because oral tolvaptan does not work in some patients, TSP may also be ineffective in certain cases. We report the case of a 74-year-old male patient with chronic heart failure and chronic kidney disease who was unresponsive to TSP. The patient underwent off-pump coronary artery bypass grafting. Initially, intravenous furosemide and oral tolvaptan were administered to manage residual fluid overload; however, intravenous furosemide was discontinued owing to a decline in serum potassium levels. Oral loop and thiazide diuretics in combination with TSP were then added to ongoing oral tolvaptan therapy, but this regimen did not achieve sufficient weight reduction. Subsequently, high-dose intravenous furosemide was reintroduced in place of oral loop diuretics, with careful monitoring for hypokalaemia. Although high-dose intravenous furosemide worsened renal dysfunction, it successfully improved fluid overload and reduced plasma B-type natriuretic peptide levels, effects that persisted even after discontinuation of TSP. This case suggests that in patients with chronic kidney disease who are unresponsive to TSP, high-dose intravenous furosemide may provide more effective management of fluid retention in heart failure, though renal function must be closely monitored.

Overweight and obesity are recognized as a public health crisis and considered a global pandemic. In adults with congenital heart disease (ACHD) it is also considered a growing menace affecting up to half of this population. In ACHD, the negative impact of obesity on cardiovascular outcomes is likely amplified by already present underlying structural and physiological cardiac abnormalities, further increasing the risk of heart failure, arrhythmias, and other cardiovascular complications. As a potentially reversible risk factor, obesity represents a clear target for improving outcomes in this already vulnerable population. While lifestyle interventions remain foundational, the use of anti-obesity medications has expanded rapidly, though evidence in ACHD remains scarce. In this state-of-the-art review, informed by a comprehensive 30-year literature overview and the expertise of an international, multidisciplinary authorship, we provide clinically practical recommendations for the judicious use of anti-obesity therapies in ACHD. This document aims to guide clinicians in real-world decision-making and serve as a foundation for future research at the intersection of obesity and congenital heart disease.

Protein lactylation, a novel posttranslational modification, has garnered significant attention for its regulatory mechanisms in cerebral ischemia-reperfusion injury. This review highlights the critical roles of protein lactylation in regulating microglia and astrocytes functions. By modulating the activation of microglia and astrocytes, inflammatory responses, and antioxidative stress, protein lactylation plays a pivotal role in neural repair and regeneration. Following cerebral ischemia-reperfusion injury, lactylation enhances the phagocytic activity of microglia, facilitates the clearance of necrotic cells, reduces the secretion of pro-inflammatory cytokines, and thus protects neurons. In astrocytes, lactylation modification supports blood-brain barrier integrity, provides nutritional support, and regulates antioxidative enzymes, further promoting neuronal survival and functional recovery. Further investigation into the molecular mechanisms of protein lactylation, its specific roles in glial cells, the development of novel lactylation regulators, and its interactions with other posttranslational modifications will offer new insights and directions for the treatment of cerebral ischemia-reperfusion injury.

Endocrine-disrupting chemicals (EDCs) are a global concern for human health and the environment. EDCs include plasticizers, pharmaceutical agents, industrial chemicals, fungicides, and pesticides. Thus, EDC exposure is a manmade consequence in our current lives. More than 1,000 chemicals are classified as EDCs, which can interfere with any aspect of the endocrine system, resulting in reproductive disorders, metabolic dysfunctions, cardiovascular diseases, neurological and immune defects, and cancers. Because EDCs affect steroid hormone regulation, there are crucial associations between EDCs and gynecological diseases. This review focuses on the inroads by which faulty signaling mechanisms and cellular responses to major EDCs, such as bisphenols (BP), phthalates, per- and polyfluoroalkyl substances (PFAS), and parabens, lead to the initiation or progression of uterine disorders, including endometriosis, leiomyoma (uterine fibroids), adenomyosis, and endometrial hyperplasia. We also summarize the features, risks, and functions of EDCs in each disease.

Intracerebral Hemorrhage (ICH) is a stroke subtype with high mortality, and its core pathological mechanism involves the disruption of cerebrovascular homeostasis. Genetic factors play a crucial role in ICH pathogenesis, underscoring the importance of identifying core regulatory factors and delineating the associated pathological network. Here, through genome-wide association study (GWAS), we identified synaptopodin (SYNPO) as a genetic susceptibility gene for ICH. SYNPO is an evolutionarily conserved actin-binding protein previously shown to be highly expressed in cerebrovascular endothelial cells, where it regulates the actin cytoskeleton to maintain endothelial junction stability. However, its functional role in ICH remains unclear. To investigate this, we conducted a synpo mutant zebrafish line using CRISPR/Cas9. Following epinephrine challenge, synpo mutant larvae displayed significantly elevated cerebrovascular leakage compared with wild-type controls, and adult mutants showed a markedly higher incidence of ICH. Transcriptomic profiling revealed significant downregulation of the key adhesion gene cdh2 in mutant brains. Subsequent rescue experiments confirmed that cdh2 mRNA supplementation effectively ameliorated the cerebrovascular leakage. In summary, our study unveils a pathway in which synpo maintains cerebrovascular homeostasis by positively regulating cdh2, demonstrating that the synpo-cdh2 axis serves as a key regulatory pathway in ICH. These findings provide insights into the genetic mechanisms underlying ICH and highlight potential therapeutic targets.

Individuals with sickle cell disease (SCD) frequently require care in the inpatient setting. Yet, there is no consensus on what comprises quality inpatient SCD care. Understanding patient, caregiver, and healthcare professional perspectives is a foundational step to defining inpatient SCD care quality.

Establish a patient, caregiver, and healthcare professional-informed foundation for quality inpatient SCD care by synthesizing qualitative literature related to the inpatient SCD care experience.

We searched Embase.com, Global Index Medicus, MEDLINE, APA PsycINFO via Ovid, Scopus, CINAHL, and Web of Science for peer-reviewed articles reporting on qualitative experiences on inpatient SCD care from inception to June 15, 2023. We dually screened studies, extracting key information from included articles before conducting thematic analysis using meta-aggregation.

We included 42 studies that explored perspectives of patients (n = 32, 7%), caregivers (n = 12, 29%), and healthcare team members (n = 9, 21%). We synthesized six meta-themes: (1) established inpatient clinical infrastructure is necessary for patient-centered inpatient SCD care, (2) comprehensive SCD care needs to wrap around all healthcare contexts, (3) enabling shared decision-making in pain management, (4) mitigating the impact of bias and stigma, (5) individualized care, (6) mental health and traumatic experiences, and (7) SCD-specific advocacy and education. Themes aligned with the Donabedian model of quality care including structural barriers (e.g., inadequate hospital staffing, limited electronic medical record access), process-related gaps (e.g., ineffective pain management, poor provider-patient communication), and outcome-driven priorities (e.g., timely pain relief, improved continuity of care).

Individuals with SCD are forced to experience and navigate the intersectional impacts of having a chronic condition from birth, a higher risk of socioeconomic disadvantage, and healthcare delivery prone to racial bias and opioid-related stigma. This review highlights key areas of quality inpatient SCD care, emphasizing the need for system-wide changes in clinical infrastructure, provider education, and patient-centered policies.

Survivors of sepsis are at high risk of developing post-intensive care syndrome (PICS), which encompasses physical, mental, and cognitive impairments after critical illness. Among these domains, physical and cognitive impairments have been linked to increased long-term mortality; however, their specific associations with mortality among patients with sepsis remain unclear. This study aimed to examine the relationship between PICS and subsequent survival, with a particular focus on physical and cognitive domains. In this retrospective cohort study, we included patients with sepsis who were admitted to the intensive care unit (ICU) for ≥ 48 hours between 2014 and 2021. Demographic and clinical data from admission, physical and cognitive impairments 1 month after ICU discharge; and 1-year survival were obtained from electronic medical records. Binary logistic regression analyses were performed to identify independent risk factors for the development of the physical and/or cognitive components of the PICS and for each individual domain. Cox proportional hazards models were used to determine the independent factors associated with 1-year mortality. Among the 210 eligible patients, 99 (47%) developed the physical and/or cognitive components of PICS, and 43 (20%) died within 1 year after ICU discharge. Physical impairment was present in 96 patients (45%) and cognitive impairment in 59 patients (28%). In the logistic regression analysis adjusted for covariates, increasing age (odds ratio [OR] 1.05, 95% confidence interval [CI] 1.02-1.09; P < .001), longer ICU stay (OR 1.09, 95% CI 1.01-1.17; P = .031), and prolonged delirium (OR 1.41, 95% CI 1.19-1.67; P < .001) were independently associated with the development of physical and/or cognitive components of PICS. In multivariable Cox analyses, the presence of these components was independently associated with higher 1-year mortality (hazard ratio 1.51, 95% CI 1.06-2.15; P = .021). When analyzed separately, physical impairment was associated with increased 1-year mortality, whereas cognitive impairment was not. Increasing age, prolonged delirium during ICU stay, and longer ICU stay were independently associated with the development of the physical and/or cognitive components of PICS. Among sepsis survivors evaluated at 1 month after ICU discharge, the presence of these components (particularly physical impairment) was independently associated with increased 1-year mortality.