Dietary guidelines represent foundational instruments of public health governance, influencing clinical practice, food assistance programs, school meal standards, and food system policies. The release of the Dietary Guidelines for Americans (DGA) 2025-2030 provides an opportunity to reassess how evolving nutrition science is translated into policy in a context characterized by high burdens of obesity and cardiometabolic disease. This review presents a comparative qualitative policy analysis of the 2025-2030 DGA and the Italian Dietary Guidelines for Healthy Eating (2018), aiming to identify structural differences and explore potential policy implications. The analysis examines governance mandates, macronutrient targets, protein sourcing, treatment of ultra-processed foods, alcohol guidance, sustainability integration, and cultural framing. Although both countries draw upon a largely shared body of scientific evidence and converge on core dietary principles, notable divergences emerge in policy emphasis and communication strategies. The DGA 2025-2030 adopt a more prescriptive approach focused on chronic disease prevention, with greater emphasis on protein intake, and explicit reference to ultra-processed foods, while sustainability remains outside the policy scope. In contrast, Italian guidelines are framed within a Mediterranean dietary pattern, emphasize plant-based protein sources and integrate environmental sustainability, food waste reduction, and cultural dimension. These differences may reflect national epidemiological and institutional contexts and variations in policy priorities. This policy review identifies policy trade-offs in guideline development and proposes actionable recommendations to enhance coherence between public health priorities, environmental sustainability, and implementation feasibility in future revisions.

Heart failure (HF) is a major global health problem and a leading cause of morbidity and mortality. In Latin America, evidence remains limited, and HF characterization in high-altitude care settings is underreported. Quito (-2,800 m a.s.l.) provides a unique clinical context, although retrospective hospital-based data without standardized hypoxia phenotyping or sea-level comparators cannot support altitude-specific causal inference.

This study aims to describe the clinical and epidemiological characteristics of patients diagnosed with HF at the Metropolitan Hospital of Quito, a tertiary care facility located at an altitude of approximately 2,800 meters, from January 2021 to December 2023.

A retrospective observational study was conducted using anonymized medical records of 122 patients diagnosed with HF (ICD-10 codes I500, I501, I509). Data on demographic, clinical, and outcome variables were collected. Exploratory comparisons were performed by discharge survival status (alive vs. deceased) using chi-square or Fisher's exact tests for categorical variables and two-sample Student's t-tests for continuous variables (two-sided p < 0.05).

Most patients (88.5%) were aged over 65 years, with men comprising 55.7% of the cohort. Hypertension (59.8%), dyslipidemia (18.9%), and atrial fibrillation (44.3%) were the most prevalent comorbidities. Hypertensive heart disease was the most frequent documented etiology of HF (14.8%), although etiology was unavailable in a substantial proportion of records. In-hospital mortality was low (3.3%). Exploratory univariate analyses identified unadjusted associations between in-hospital mortality and dialysis dependency, immunologic diseases, and other vascular diseases.

This study provides a contemporary clinical and epidemiological profile of HF patients managed at a high-altitude tertiary hospital in Quito and identifies exploratory factors associated with in-hospital mortality in this care setting. Future multicenter studies incorporating standardized hypoxia-related measurements and appropriate comparator cohorts are needed to better understand HF phenotypes and outcomes in Andean populations.

This study aims to explore the associations of artificial intelligence (AI)-derived coronary CT angiography (CCTA) features with coronary flow reserve (CFR) measured by cardiac-cadmium zinc-telluride single-photon emission computed tomography (CZT-SPECT) and CT-derived fractional flow reserve (FFR-CT), and to investigate their intrinsic relationships.

This retrospective study included 251 patients (753 vessels) with suspected or known coronary artery disease (CAD), who underwent CZT-SPECT and concurrent CCTA. Myocardial ischemia was defined as CFR <2.0 or FFR-CT ≤0.8. Generalized estimating equations (GEE) were used to analyze the associations between CCTA coronary parameters and the two ischemia definitions.

Among the 753 vessels, the agreement analysis between CFR and FFR-CT for ischemia was poor (Kappa = 0.084). Multivariate analysis demonstrated that CFR <2.0 was only associated with perivascular fat attenuation index (FAI) and calcified plaque burden, whereas FFR-CT ≤0.8 was additionally predicted by low attenuation plaque and lipid plaque burden (all p < 0.05). Subgroup analysis revealed distinct plaque feature patterns among discordant CFR/FFR-CT statuses. The same set of coronary features achieved an adjusted AUC of 0.892 for FFR-CT-defined ischemia and 0.615 for CFR-defined ischemia.

CFR and FFR-CT reflect different pathophysiological dimensions: CFR reduction is more associated with microvascular dysfunction in the context of inflammation and diffuse lesions, whereas FFR-CT mainly reflects focal, obstructive ischemia caused by high-risk plaques (such as low attenuation plaque). CCTA is an important tool for assessing obstructive coronary lesions, but coronary features alone are insufficient to predict whether CFR is abnormal or not. However, in the absence of invasive reference standards (invasive FFR and index of microcirculatory resistance), these findings should be considered hypothesis-generating and require confirmation in future studies incorporating invasive physiological assessment.

Insomnia is a prevalent health issue within the general population. Nonetheless, there is a paucity of research specifically addressing chronic insomnia among hospitalized patients. Consequently, the objective of this study is to investigate chronic insomnia in adult inpatients.

A retrospective analysis was conducted on hospitalized patients at Fengjie County People's Hospital in Chongqing from January 2022 to June 2025. The study included patients aged 18 to 100 years, with comprehensive documentation of their demographic information, laboratory test results, and insomnia treatment details. Patients with incomplete data or those under 18 years of age were excluded from the study. The analysis focused on the age distribution, gender ratio, and BMI distribution of the patients, as well as the prevalence of primary diagnostic categories and the distribution characteristics of fasting blood glucose levels and dyslipidemia.

The study included a total of 871 patients, with a male representation of 39.6%. The mean body mass index (BMI) was 23.1 ± 3.7 kg/m², and the mean age was 64.1 ± 13.9 years. The predominant sources of disease were identified as infectious diseases, cardiovascular diseases, neurological disorders, tumors, and musculoskeletal conditions. A significant proportion of patients presented with elevated fasting blood glucose levels and dyslipidemia.

Chronic insomnia in hospitalized patients predominantly affects elderly women. Chronic insomnia in hospitalized patients predominantly affects elderly women, who primarily present with infectious diseases, cardiovascular conditions, neurological disorders, tumors, and musculoskeletal issues. These patients often exhibit dyslipidemia and elevated fasting blood glucose levels, necessitating clinical attention.

Atherosclerosis (AS) is a major underlying cause of cardiovascular disease. Rupture of unstable atherosclerotic plaques can induce severe acute cardiovascular events and sudden cardiac death. Therefore, developing targeted interventional therapies for atherosclerotic plaques is clinically important to improve cardiovascular mortality. With the advancement of nanomedicine, nanomaterials have demonstrated great potential in atherosclerosis treatment due to their unique compositional/structural features, synthesis strategies, and surface modifications. Based on the pathological characteristics of atherosclerotic plaques, the design and preparation of stimulus-responsive, surface-functionalized, and conditionally-released nanomaterials have become an important approach to achieving precise intervention for atherosclerotic lesions. Considering the pathological features of different cell types involved in AS progression, this review describes the targeting strategies, structural and functional designs, and potential mechanisms of action of targeted nanotherapies in the treatment of atherosclerosis. By summarizing representative recent studies in detail, we reveal the intrinsic interactions and relationships between current targeted nanotherapies and atherosclerotic plaques. Finally, this review provides an outlook on the future application of nanomaterials by presenting key scientific questions that have not yet been addressed, to advance the clinical translation of targeted nanotherapies for atherosclerosis.

While glucose-lipid metabolic remodeling is recognized as a major contributor to cardiomyocytes proliferation, the role of amino acid metabolism in cardiac regeneration remains poorly understood. In this study, glycine was identified as a previously unrecognized pro-proliferative amino acid.

Primary cardiomyocytes, neonatal mice, and adult mouse models of myocardial infarction were employed to investigate the pro-proliferative effects of glycine on cardiomyocytes. Cardiomyocyte proliferation was assessed by immunofluorescence staining of cell-cycle-related markers. Cardiac function was evaluated by echocardiography, and histopathological alterations were examined using Masson's trichrome staining. To overcome the pharmacokinetic limitations of free glycine and enhance therapeutic efficacy, a cardiac-targeted liposomal nanoformulation (LNP@Gly) was developed and applied in vivo. Mechanistic studies were performed using RNA sequencing, Western blotting, co-immunoprecipitation (co-IP), immunostaining, pharmacological inhibition and activation approaches.

Exogenous glycine supplementation (700 mg/kg) consistently enhanced cardiomyocyte proliferation across in vitro, neonatal, and adult myocardial infarction models. In infarcted adult hearts, glycine supplementation further improved cardiac function and reduced myocardial fibrosis. A cardiac-targeted liposomal formulation of glycine (LNP@Gly) effectively overcame the pharmacokinetic limitations of free glycine and achieved enhanced therapeutic efficacy at a substantially lower dose (4 mg/kg). At the molecular level, glycine treatment was associated with increased AKT phosphorylation, reduced GCN2 activation, and weakened GCN2-AKT interaction. Pharmacological modulation further supported a critical role for the GCN2-AKT axis in glycine-induced cardiomyocyte proliferation and cardiac repair.

These findings identify glycine as a novel metabolic regulator of cardiomyocyte proliferation and cardiac regeneration through modulation of the GCN2-AKT signaling axis. Moreover, the integration of amino acid-specific metabolic regulation with cardiac-targeted nanodelivery represents a translatable therapeutic strategy for ischemic heart disease.

Postoperative atrial fibrillation (AF) remains a common and morbid complication of cardiac surgery, driven by inflammation and fibrosis for which targeted therapies are limited. Conventional antiarrhythmic and anticoagulant strategies have little impact on its incidence or recurrence. We previously demonstrated that a single intracardiac injection of extracellular vesicles (EVs) derived from human heart explant-derived cells prevents postoperative AF in preclinical models. The present study aimed to elucidate the mechanisms underlying this protective effect in human cells.

Induced pluripotent stem cells (iPSCs) were generated from circulating mononuclear cells obtained from cardiac surgery patients at high and low risk for postoperative AF, then differentiated into atrial fibroblasts. These cells were compared with primary human atrial fibroblasts isolated from surgical tissue. Clinical-grade cardiac EVs were manufactured from heart explant-derived cells and characterized for size, surface markers, and microRNA cargo. Both iPSC-derived and primary fibroblasts were exposed to inflammatory (IL-6, TGF-β1, lipopolysaccharide) and fibrotic stimuli, with or without EV treatment. Inflammasome activation and cytokine secretion were assessed by transcript and protein analyses.

iPSC-derived and primary atrial fibroblasts exhibited comparable antigenic and functional profiles and efficiently internalized cardiac EVs. EV treatment markedly suppressed activation of the NLRP3 inflammasome following lipopolysaccharide and nigericin stimulation, resulting in reduced secretion of Caspase-1, IL-1β, and IL-18 and corresponding transcript downregulation. EVs also attenuated IL-6 and TGF-β1 induced fibroblast proliferation, confirming their anti-inflammatory and antifibrotic effects across cell sources and patient risk groups.

This study establishes a patient-specific human cellular model of cardiac fibrosis, a key determinant of postoperative AF, and identifies heart-derived EVs as potent suppressors of inflammasome activation and profibrotic signaling. These findings provide mechanistic insight into the anti-inflammatory and antifibrotic actions of cardiac EVs and support their further development as a cell-free biologic for the prevention of postoperative AF.

Social isolation is a known modifiable risk factor for many chronic diseases including cardiovascular, metabolic, and brain disorders. Recent research has demonstrated that social isolation is similarly detrimental to skeletal health, but these effects may be sexually dimorphic. In rodents, isolation negatively affects bone in adult male mice, but not in females. However, these sex differences have not been systematically investigated, and it is unknown if they persist with long-term social isolation. The goal of our study was to investigate if isolation-induced bone loss may occur on different timescales between female and male mice, as well as investigate the potential roles of estrogen and testosterone. We examined bone changes in grouped (4 mice/cage) or isolated (1 mouse/cage) female and male 16-week-old C57BL/6J mice after 2, 4, or 8 weeks of treatment. We found that social isolation through single housing significantly reduced bone parameters across treatment lengths in male mice (20% reduction in Tb.BV/TV; 8% reduction in Ct.Th.) but not in females even with prolonged isolation. Isolation also decreased biomechanical properties in the femur of male but not female mice. While the females' overall bone phenotype was unaffected, isolated females did show an increase in bone turnover markers with as little as 2 weeks of isolation. Isolation also altered estrogen-related gene expression in male mice isolated for 4 or 8 weeks. Overall, our results demonstrate that short- and long-term social isolation has sexually dimorphic effects on murine bone. These findings have important clinical implications for individuals at risk for social isolation, as well as for pre-clinical rodent models utilizing single housing.

Ferroptosis is an iron-dependent form of regulated cell death driven by unrestrained lipid peroxidation, morphologically and biochemically distinct from apoptosis, necrosis, and autophagy. It is increasingly recognized as a core pathophysiological mechanism across the full spectrum of cardiovascular diseases, including myocardial ischemia-reperfusion injury, heart failure, atherosclerosis, diabetic cardiomyopathy, and chemotherapy-induced cardiotoxicity. The initiation and progression of ferroptosis are governed by the dysregulation of iron homeostasis, lipid metabolic remodeling, and collapse of antioxidant defense systems, with extensive crosstalk with other regulated cell death modalities in cardiovascular pathophysiology. Preclinical studies have consistently demonstrated that targeting ferroptosis exerts robust cardioprotective effects via multiple mechanisms. However, clinical translation faces key hurdles, including the lack of specific biomarkers, off-target risks, and interindividual heterogeneity in therapeutic response. This review systematically summarizes the regulatory mechanisms of ferroptosis, its causal role in cardiovascular diseases, and the latest advances in targeted therapeutic strategies, with a focus on clinical translation prospects and challenges.

Immune checkpoint inhibitors (ICIs) are prone to induce cardiovascular adverse reactions during the immunotherapy of cancer patients, among which ICIs-related myocarditis is the most severe. Mitophagy dysregulation is associated with various heart diseases, but its role in ICIs-related myocarditis remains unclear.

Mitophagy key genes in ICIs-related myocarditis were screened based on the single-cell RNA sequencing and bulk RNA sequencing data, and their expression levels and diagnostic value were verified. Meanwhile, the key genes, trajectory analysis and cell interaction were validated at the single-cell level. Finally, the myocardial injury markers, cardiac function indicators, histopathological analysis and mitophagy key genes were verified by constructing a mouse model of ICIs-related myocarditis.

A total of 4 mitophagy key genes in ICIs-related myocarditis were identified by combining multiple bioinformatics analysis methods: AW112010, Igfbp7, Tmsb4x, Ost4. The expression levels of mitophagy key genes in the ICIs-related myocarditis group were significantly higher than those in the normal group (P < 0.05 or P < 0.01), and both had high diagnostic value. Trajectory analysis and cell interaction results showed the interaction intensity and relative expression patterns among these 4 key genes. The ICIs-related myocarditis mouse model showed elevated myocardial injury markers (BNP, CK-MB, cTnT) and decreased cardiac function indicators (LVEDV, LVEF, LVIDd, LVIDs) compared to the normal group (P < 0.05 or P < 0.01). The pathological sections revealed obvious inflammation and damage in the myocardium of myocarditis group mice. Additionally, the qRT-PCR results indicated that the expression levels of AW112010, Igfbp7, Tmsb4x and Ost4 were significantly higher than those in the normal group (P < 0.05 or P < 0.01).

Mitophagy is involved in the pathogenesis of ICIs-related myocarditis, and AW112010, Igfbp7, Tmsb4x and Ost4 may become potential biomarkers for future clinical practice.