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Time-of-day, satellite cells, and velocity collectively influence ex vivo isovelocity force production in mouse extensor digitorum longus muscle.
Physiol Rep
Ryan E Kahn, Sudarshan Dayanidhi, Richard L Lieber
Skeletal muscles are exquisitely designed to produce force that facilitate movement. Circadian "molecular clocks" residing in muscle play a role in regulating force production with muscle stem cell (satellite cells, SC) molecular clocks modulating isometric and eccentric force according to time-of-day. However, many tasks of daily living and exercise (i.e., walking/running) involve force and power produced during muscle shortening. Thus, the purpose of this study was to determine whether isovelocity forces and power are also modulated by SCs according to time-of-day. Using previously published samples (a mouse model capable of SC ablation), we evaluated isovelocity forces across a range of velocities (1-11 Lf/s) at two different times of day ZT1, ZT9 in the presence and absence of SCs. The main finding of this investigation was that isovelocity force production is regulated by a third-order interaction effect between time-of-day × SCs × velocity (p < 0.001). Additionally, a significant effect of time-of-day was observed for isovelocity force and power when comparing ZT1 vs. ZT9 SC+ mice whereas this effect was absent in SC- animals. These results suggest SCs harbor a time-of-day and velocity dependent effect on isovelocity force production and power. Further work is required to elucidate the underlying mechanisms of this phenomenon.
Skeletal Fiber Type in Muscle Pain and Dysfunction.
Biomedicines
Maria Lopes Cardia, Bruno Daniel Carneiro, Isaura Tavares +1 more
Different types of skeletal muscle fibers display marked heterogeneity in metabolic, mechanical, and regenerative properties. However, their role in chronic musculoskeletal pain remains insufficiently integrated into clinical models. Chronic pain is associated with altered neuromuscular control, prolonged low-level activation, and reduced recruitment of high-threshold motor units. These factors may promote fiber type-specific remodeling. This narrative review critically synthesizes current evidence on the relationship between musculoskeletal pain and muscle fiber types. The focus was on metabolic vulnerability, mechanical susceptibility, and regenerative capacity. A structured literature search was conducted in PubMed, Scopus, and Web of Science, focused on human studies and key translational models. Chronic musculoskeletal pain is characterized by acquired fiber type-specific adaptations rather than a fixed unfavorable profile. In chronic pain scenarios, Type I fibers present features of chronic overload, including hypertrophy with insufficient capillarization and increased satellite cell activity. Type II fibers exhibit relative disuse, atrophy, and reduced satellite cell content, resembling accelerated muscle aging. Symptom duration, neuromuscular control strategies, and task-specific loading patterns modulate these adaptations, with interindividual variation. Muscle dysfunction in chronic pain reflects maladaptive but potentially reversible neuromuscular and histological plasticity. These findings indicate that rehabilitation strategies should be individualized, involving context-specific exercise strategies to restore muscle structure, function, and regenerative potential in chronic musculoskeletal conditions.
Overexpression of IGF2 Alters the Transcriptional Profile of Goose Skeletal Muscle Satellite Cells.
Biomolecules
Cui Wang, Yi Liu, Yunzhou Yang +2 more
Insulin-like growth factor 2 (IGF2) plays a pivotal role in regulating growth and development; however, its functional involvement in skeletal muscle satellite cells (SMSCs) remains incompletely understood. To elucidate the regulatory role of IGF2, goose SMSCs were engineered to overexpress IGF2 via lentiviral transduction, followed by comprehensive transcriptomic profiling. Comparative analysis revealed 2802 differentially expressed genes (DEGs) in IGF2-overexpressing cells relative to controls, comprising 1202 upregulated and 1600 downregulated genes. IGF2 overexpression markedly activated fibrogenic programs, as evidenced by the upregulation of AP-1 complex components (FOS, JUN), extracellular matrix-related genes (COL1A1, COL5A3), and Wnt signaling receptors (FZD1, FZD7). In contrast, genes involved in myogenic differentiation and contractile function were broadly suppressed, including key myogenic transcription factors (MEF2C, MEF2D), sarcomeric structural proteins (MYBPC1, ACTN2, MYOM3), and metabolic enzymes. Through the construction of protein-protein interaction networks coupled with functional enrichment analysis, we observed a concerted suppression of myogenic regulatory networks critical for myofiber formation. Quantitative real-time PCR validation further confirmed the reliability of the transcriptomic data. Collectively, these findings suggest that overexpression of IGF2 induces a phenotypic shift from myoblasts toward a fibroblast-like state, uncoupling proliferation from differentiation while enhancing fibrogenic identity. This study provides novel insights into IGF2-mediated regulatory mechanisms underlying skeletal muscle development and fibrotic processes.
Cancer cell migration under control of human cathelicidin LL-37.
Biomed Pharmacother
Konrad Żochowski, Maja Sadowska, Ewelina Piktel +2 more
Cancer cell migration is a key step in the metastatic cascade. Understanding its mechanisms represents one of the greatest challenges in modern oncology. Both in vitro and in vivo experimental models and mathematical descriptions of movement dynamics are used to study this complex phenomenon. These models allow for the quantitative characterization of movement trajectories based on cell motion parameters. Within the tumor microenvironment, the human cathelicidin LL-37 holds a special place as a regulator of these processes. This article summarizes current knowledge (until July 2025) on LL-37's involvement in cancer cell migration across several cancer types. LL-37 has been implicated in tumor progression through modulation of signaling pathways, epithelial-mesenchymal transition, and angiogenesis, highlighting it as a potential target for research into mechanisms of cancer invasion and metastasis. LL-37 serves as an agonist of multiple receptors, initiating signaling pathways. Its effects are highly dependent on the tumor type, receptor expression, concentration, and exposure time. Data show that in most studied epithelial tumors, including breast, hepatocellular, and squamous cell carcinomas, LL-37 typically promotes cell migration and invasiveness. However, in glioma and colon cancer (being a notable epithelial exception) this peptide inhibits motility. Understanding mechanisms of LL-37 action opens new perspectives in the search for therapeutic strategies aimed at controlling the invasiveness and metastatic potential of tumor cells. At the same time, the more widespread use of mathematical models in medicine creates the prospect of developing effective therapies that inhibit the ability of cancers to metastasize.
Vitamin D boosts HIV-1 resistance in female genital epithelial cells by enhancing antiviral cathelicidin expression.
Front Immunol
Sandra M Gonzalez, Wbeimar Aguilar-Jimenez, Maria T Rugeles +4 more
Elevated levels of serum Vitamin D (VitD) and increased expression of its receptor on peripheral blood cells have been reported in individuals who have been exposed to HIV-1 yet remain seronegative (HESN). This study aimed to investigate the potential antiviral role of VitD in the female genital epithelium, which constitutes the first physical barrier against HIV-1. We hypothesized that VitD may modulate susceptibility to HIV-1 infection by influencing epithelial functions such as tight junction integrity, production of antiviral peptides, and secretion of pro-inflammatory mediators.
Management of Obese Patients with Cardiovascular Disease with Emerging Weight-Lowering Drugs: A Narrative Review.
Biomedicines
Alessandro Ciarloni, Gianmaria Salvio, Monia Bordoni +2 more
Background/Objectives: Obesity has a huge impact on global healthcare and economy. Consequently, the pharmaceutical industry has recently introduced novel anti-obesity drugs such as semaglutide and tirzepatide, which can yield remarkable weight reduction in patients, while also having significant cardiovascular benefits. Methods: Other weight-lowering medications are currently under investigation, and this narrative review provides an overview of the main novel drugs that are being tested. Results: These novel agents have different mechanisms of action, e.g., calorie intake reduction, increase in basal metabolism, and increase in muscle mass. Conclusions: In the future, obesity treatment is likely to become increasingly personalized, and further cardiovascular benefits could be expected. The combined use of different molecules could minimize their side effects, for instance, by minimizing muscle wasting observed during glucagon-like peptide 1 receptor agonists (GLP1-RAs) therapy. In our opinion, these highly effective drugs could represent a valuable addition to healthy lifestyle, as the evidence linking increases in muscle mass and basal metabolic rate to improved cardiovascular health is strongest when these changes are achieved through diet and regular physical activity.
Once-Weekly Semaglutide in Patients with Cardiovascular-Kidney-Metabolic Syndrome: A Real-World Study.
Pharmaceuticals (Basel)
Alicia Trenas-Calero, Nuria Prieto-Laín, Ana I Gómez-Hernández +6 more
Introduction and Objectives: There is limited evidence on the role of glucagon-like peptide-1 receptor agonists in the interplay between cardiovascular disease, chronic kidney disease, and metabolic dysfunction. This work analyzed the efficacy and safety of once-weekly semaglutide in patients with cardiovascular-kidney-metabolic syndrome. Patients and Methods: This observational, real-world study included patients with heart failure, chronic kidney disease, obesity, and type 2 diabetes mellitus treated with once-weekly semaglutide (Sema-CKM Group) and patients not treated with glucagon-like peptide-1 receptor agonists (Control-CKM Group). A 1:1 propensity score matching analysis was performed. The two primary outcomes were heart failure events and major kidney disease events at 24 months. Results: After matching, 302 patients were included in each group. A heart failure event occurred in 63 patients (20.9%) in the Sema-CKM Group and 121 (40.1%) in the Control-CKM Group (OR: 0.80; 95%CI: 0.62-0.98; p < 0.01). The number of major kidney disease events was lower in the Sema-CKM Group than the Control-CKM Group (36 vs. 65; OR: 0.85; 95%CI: 0.72-0.98; p = 0.014). Patients in the Sema-CKM Group were more likely to have an improvement in heart failure health status from baseline to 24 months (OR: 2.80; 95%CI: 1.30-4.30; p < 0.01). Semaglutide also improved glycemic control (glycated hemoglobin -0.7%) and reduced body weight (-9.3 kg). Conclusions: Once-weekly semaglutide was associated with reductions in heart failure events and major kidney disease events in patients with heart failure, chronic kidney disease, obesity, and type 2 diabetes mellitus. Further research on glucagon-like peptide-1 receptor agonists in cardiovascular-kidney-metabolic syndrome is needed.
Quality by Design-Based Formulation Development of an Oral Semaglutide Tablet.
Pharmaceutics
Ji-Hyeon Yoon, Do-Hyub Kim, Joo-Eun Kim
Background: This study aimed to investigate, from a scientific and formulation perspective, an oral semaglutide tablet incorporating sodium caprate (C10) as an intestinal absorption enhancer and to optimize its formulation performance using a Quality by Design (QbD)-based approach. Semaglutide-a peptide-based therapeutic-provides effective glycemic control and weight reduction; however, its extremely low oral bioavailability has limited administration to subcutaneous injection. Although various attempts have been made to improve peptide absorption, achieving consistent delivery through oral routes remains a significant challenge due to enzymatic degradation and poor membrane permeability. Methods: To overcome these limitations, an absorption enhancer (sodium caprate) was incorporated to enhance oral absorption, and a Quality by Design (QbD)-based approach was applied to systematically guide formulation development. Following the definition of the Quality Target Product Profile and critical quality attributes, risk assessments (Preliminary Hazard Analysis and Failure Mode and Effects Analysis) were conducted to identify key formulation factors. A design of experiments approach was then employed to determine the optimal tablet composition. Results: Consequently, the resulting formulation met all predefined quality criteria, including hardness, disintegration, friability, and content uniformity. In addition, the in vitro dissolution profile demonstrated a release pattern comparable to that of the reference product, with similarity factor values of 74.4, 74.7, and 71.3 at pH 1.2, 4.0, and 6.8, respectively. Conclusions: These findings indicate that the formulation can achieve consistent and reproducible quality performance as an oral semaglutide dosage form. The QbD-based formulation design strategy presented in this study provides a robust and broadly applicable approach for developing oral delivery systems for peptide drugs, including semaglutide, and ultimately provides useful formulation insight for future peptide-based oral delivery research.
Acute Contractile Effects of Glucagon-like-Peptide-1 Receptor Agonists in the Human Heart.
Pharmaceutics
Joachim Neumann, Uwe Kirchhefer, Britt Hofmann +1 more
Glucagon-like-peptide-1 receptor (GLP-1R) agonists are under development as new drugs to treat type 2 diabetes, liver disease, obesity and cardiovascular diseases. Some of these drugs are solely agonists of the GLP-1R. It turned out that their benefit could be improved when they also stimulated the glucagon receptor (GCGR) and/or the glucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR). Stimulation of GLP-1R in cell cultures but also in neonatal atrial and/or ventricular cardiomyocytes and adult atrial cardiomyocytes raised the activity of adenylyl cyclase and thus augmented the 3',5'cyclic adenosine monophosphate (cAMP) levels. We discuss here the acute contractile effects of such agonists on isolated human atrial and ventricular cardiac preparations from failing and non-failing hearts. We address the receptors involved, GLP-1R expression in various cardiac regions of the human heart, single and multiple receptor agonists and the post-receptor signal transduction system of the GLP-1R in the human heart. Some of the new drugs addressed are still in the early phases of clinical development. We critically discuss the experimental and clinical data available and we also define research needs for experimental and clinical studies.
Dercum Disease: Exploratory Therapeutic Approaches in the Absence of Standardized Medical Treatment-A Single Center Case Series.
Life (Basel)
Alessandro Magnatta, Alice Verdelli, Virginia Corti +14 more
Dercum's disease (DD) is a rare chronic disorder characterized by painful subcutaneous lipomas, mostly affecting overweight or obese middle-aged women. The etiology remains unclear, and evidence for medical treatments is limited. Surgical approaches may reduce pain but are associated with frequent relapses and are difficult to implement in extensive clinical pictures. We investigated the outcomes of multiple medical and surgical therapeutic strategies. Particularly, we explored immunomodulators (methotrexate and infliximab), used alone or combined with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) such as semaglutide, as well as the dual GIP (glucose-dependent insulinotropic polypeptide)/GLP-1 RAs tirzepatide. Five patients with DD were included in this retrospective single-center case series. Baseline clinical data, medical history, and longitudinal information on Dermatology Life Quality Index (DLQI), Visual Analogue Scale (VAS) for pain, and body mass index (BMI) were collected from existing medical records and scheduled follow-up visits conducted since 2021. Clinical trajectories differed across patients and regimens. Methotrexate and infliximab coincided with variable and often transient improvements in pain and quality of life. Combination regimens including GLP-1 RAs were accompanied by weight reduction and, in selected patients, by sustained improvements in pain and DLQI. In other cases, the benefit was limited or absent. Adverse events were manageable and consistent with the known safety profiles of these drugs. In this small real-world case series, therapeutic responses in DD were highly individualized, underscoring the absence of standardized medical treatment and the need for patient-tailored strategies. The observed patterns suggest that immunomodulatory and incretin-based therapies may represent exploratory options in selected patients, especially when surgery is not feasible. However, controlled studies are needed to clarify their role.
Three-year changes in renal function after switching from injectable GLP-1 receptor agonists to oral semaglutide in Japanese patients with type 2 diabetes: a retrospective cohort study.
Diabetol Int
Satoru Takashima, Kanji Terui, Fukuko Yamada +1 more
While the FLOW trial established the renoprotective effects of subcutaneous semaglutide, real-world evidence regarding the long-term renal effects of therapeutic switching from injectable glucagon-like peptide-1 receptor agonists (GLP-1RAs) to oral semaglutide remains limited. We evaluated long-term changes in renal function following this therapeutic switch.
The Interplay Between GLP-1-Based Therapies, the Gut Microbiome, and MASLD/MASH in Type 2 Diabetes Mellitus: A Narrative Review.
Biomedicines
Boris Dinkov, Diana Pendicheva-Duhlenska
GLP-1-based drugs are approved for the treatment of type 2 diabetes mellitus (T2DM) and obesity. Metabolic dysfunction-associated steatotic liver disease (MASLD) affects more than 60% of patients with T2DM, and the gut microbiome plays a critical role in its pathogenesis. The gut-liver axis represents a key mechanistic link between dysbiosis and hepatic steatosis. A narrative literature review was conducted using PubMed, Scopus, and ClinicalTrials.gov (2015-2026). Search terms included "GLP-1 receptor agonist," "microbiome," "MASLD," "MASH," "NAFLD," "NASH," "liraglutide," "semaglutide," "tirzepatide," "dulaglutide," and "exenatide." Of 363 identified articles, 330 were excluded due to duplication or non-relevant study design; 33 studies (18 preclinical, 15 clinical) were included. In preclinical models, liraglutide demonstrated normalization of the Firmicutes/Bacteroidetes ratio and increased Bifidobacterium and Lactobacillus spp., while tirzepatide significantly reduced hepatic steatosis and increased Akkermansia abundance in diabetic mice. Semaglutide improved gut barrier integrity, increased Alloprevotella and Alistipes, and ameliorated MASLD in murine models. In clinical studies, tirzepatide achieved MASH resolution in 44-62% of patients in the phase 2 SYNERGY-NASH trial. In August 2025, the FDA approved semaglutide for MASH with fibrosis based on the Phase 3 ESSENCE trial. A recent longitudinal study in T2DM patients showed that baseline microbiome composition predicted glycemic response to semaglutide, without significant changes in microbiome diversity. In conclusion, GLP-1-based therapies demonstrate consistent preclinical associations with gut microbiome modulation and reduction in hepatic steatosis. Baseline microbiome composition has been suggested as a potential predictor of treatment response, supporting a personalized approach to MASLD management and warranting future clinical studies.
The Role of Cellular Senescence in Obstructive Airway Diseases: From Mechanisms to Therapeutic Targets.
Int J Mol Sci
Argyro Vrouvaki, Marina Moustaka Christodoulou, Georgios Hillas +2 more
Cellular senescence is a stress-induced type of irreversible cell cycle arrest, driven by telomere attrition, oxidative stress, DNA damage, mitochondrial dysfunction, oncogene activation, and chronic inflammation. Senescent cells remain metabolically active, secreting cytokines, chemokines, growth factors, matrix metalloproteinases, extracellular vesicles and oxidative mediators, comprising a senescence-associated secretory phenotype (SASP) that affects the tissue microenvironment. With aging, impaired immune clearance results in senescent cell accumulation, promoting inflammation, immunosuppression and fibrosis. Emerging evidence implicates cellular senescence in obstructive airway diseases, reflecting the lung's continuous exposure to environmental and oxidative insults, and several pathways, including DNA damage response and p53/p21 and p16INK4a signaling, telomere dysfunction, reactive oxygen species production, and mitochondrial defects, integrate stress signals to enforce senescence. In chronic obstructive pulmonary disease, a SASP-associated inflammatory milieu supports stress-induced tissue injury, while uncertainty still exists about the effects of chronic SASP on tumor suppression versus tumor promotion. In asthma, senescence processes have been associated with both Type(T)2-high and T2-low endotypes, underlying the interplay between environmental exposures, airway epithelial dysfunction and induced senescence mechanisms. Finally, in bronchiectasis, the neutrophilic, dysbiotic airway environment links dysregulated senescence with disease persistence and progression. Conventional therapies, antioxidants, serine protease inhibitors and novel senotherapeutic strategies represent promising approaches for therapeutic interventions.
A composite measure of cerebral small vessel disease predicts cognitive change after stroke.
medRxiv
Mahir H Khan, Stuti Chakraborty, Octavio Marin-Pardo +15 more
Post-stroke cognitive recovery is difficult to predict using focal lesion characteristics alone. The brain's capacity to maintain cognitive function depends also on structural integrity of the whole brain. One way to measure brain health is through the severity of cerebral small vessel disease (CSVD) markers, which reflect aging-related pathologies that erode structural integrity. Here, we propose a composite measure of CSVD (cCSVD) integrating three independently validated biomarkers automatically quantified using T1-weighted MRIs: white matter hyperintensity volume (WMH; representing vascular injury), perivascular space count (PVS; putative glymphatic clearance), and brain-predicted age difference (brain-PAD; structural atrophy). We hypothesize that cCSVD, which captures the shared variance across these CSVD biomarkers, will be a robust indicator of whole-brain structural integrity and predict cognitive changes 3 months after stroke. We analyzed 65 early subacute stroke survivors with assessments within 21 days (baseline) and at 90 days (follow-up) post-stroke. WMH volume, PVS count, and brain-PAD were quantified from baseline T1-weighted MRIs, and then residualized for age, sex, days since stroke, and intracranial volume. Principal component analysis (PCA) of the residualized biomarkers was used to derive cCSVD. Beta regression with stability selection using LASSO was used to model three outcomes: baseline Montreal Cognitive Assessment (MoCA) scores, follow-up MoCA scores, and longitudinal change (follow-up score adjusted for baseline score). Logistic regression was used to test if baseline cCSVD predicted improvement in those with baseline cognitive impairment (MoCA < 26). The PCA revealed that the first principal component (PC1) explained 43.1% of the total variance among WMH volume, PVS count, and brain-PAD. The three biomarkers contributed nearly equally to PC1, which was subsequently used as the baseline cCSVD score. Lower baseline cCSVD was significantly associated with better MoCA scores at follow-up (β = -0.19, p = 0.009), even after adjusting for baseline MoCA (β = -0.12, p = 0.042), and, importantly, outperformed all individual biomarkers. Furthermore, lower cCSVD at baseline significantly increased the likelihood of improving to cognitively unimpaired status at three months (OR = 0.34, p = 0.036), independent of age and education. The composite CSVD captures the additive impact of vascular injury, glymphatic dysfunction, and structural atrophy on recovery in a way that individual measures do not. cCSVD accounts for shared variance across these domains, reflecting a patient's latent capacity for cognitive recovery, where relative integrity in one CSVD domain may mitigate effects of another. This automated, T1-based framework offers a scalable tool for predicting post-stroke recovery.
Altered cerebrospinal fluid-based clearance mechanisms in aging autistic adults.
Res Sq
Danielle Christensen, Giuseppe Barisano, Bradley J Wilkes +8 more
Autistic adults demonstrate a 4-6-fold increased risk of unspecified dementia compared with the general population; however, the neurobiological substrates underlying this elevated risk remain unexplored. Alterations in cerebrospinal fluid-based mechanisms involved in brain metabolic waste clearance may represent a shared neuropathological pathway between autism spectrum disorder and dementia. Specifically, developmental deviations in cerebrospinal fluid-related imaging markers have been consistently reported in autistic infants, children, and adolescents, and brain amyloid and other metabolic waste accumulation is a hallmark of Alzheimer's disease and related dementias. Despite this overlap, cerebrospinal fluid-based regulatory mechanisms have not been systematically examined in ageing autistic adults. Here, we used a multimodal magnetic resonance imaging approach to quantify structural and diffusion-based markers of cerebrospinal fluid regulation in middle-aged and older autistic adults compared with matched controls.
Bacterial Extracellular Vesicles in Aging: Mechanisms and Therapeutic Prospects.
Int J Nanomedicine
Junfei Tan, Muhammad Zubair, Lin Zhang +5 more
Bacterial extracellular vesicles (bEVs) are increasingly recognized as critical mediators of gut-host interactions; however, their specific role in the aging process remains obscured by fragmented data and disease-specific silos. Current understanding lacks a cohesive mechanism that explains how age-related physiological changes transform bEVs from commensal signals into systemic drivers of pathology. This review synthesizes disparate findings to elucidate a synergistic mechanism: aging compromises intestinal barrier integrity, facilitating bEV translocation, while simultaneously impairing immune clearance capabilities (e.g. loss of Vsig4+ Kupffer cells), leading to their toxic accumulation. We resolve conflicting reports on bEV functionality-such as the paradoxical pro-calcific effects of Lactobacillus rhamnosus GG-derived vesicles in chronic kidney disease-by contextualizing them within the host's aging microenvironment. Beyond mapping these interactions across the gut-brain, metabolic, cardiovascular, and bone axes, we identify specific cargo molecules, such as lipopolysaccharide (LPS), curli, and bacterial DNA, that fuel inflammaging. However, translating these insights into therapeutic applications faces significant challenges, including methodological heterogeneity in isolation protocols and unresolved immunogenicity risks. By outlining a strategic roadmap for standardization and rigorous clinical validation, this study redefines bEVs not merely as biomarkers but as actionable targets for delaying aging and mitigating age-related diseases.
Vascular Aging.
Circulation
Ruoqi Wang, Stephen Y Chan, Toren Finkel
Vascular aging is a central determinant of healthy life span, not only influencing the susceptibility to cardiovascular diseases but also shaping the risk of systemic decline across multiple organs. It is driven by a variety of age-related factors, including cellular senescence, chronic inflammation, loss of proteostasis, mitochondrial dysfunction, genomic instability, epigenetic remodeling, and stem cell exhaustion. These processes interact with the unique mechanical and metabolic environment of the vasculature to create a distinctive pathological trajectory, manifested in part as arterial stiffening, impaired barrier integrity, and dysregulated vasomotor control. Recent advances in single-cell omics and cross-organ molecular clocks have revealed the heterogeneity and organ specificity of aging, underscoring the need for integrative frameworks that connect vascular biology with overall health. Meanwhile, the development of diverse therapeutic strategies-ranging from senolytic and immune-mediated clearance to metabolic and mitochondrial interventions-highlights the translational potential of targeting the aging vasculature. Looking ahead, multimodal biomarkers and precision medicine may transform vascular aging from an inevitable process into a modifiable determinant of health span.
Effect of Yiqi Fumai lyophilized injection on B-type natriuretic peptide levels in patients with acute decompensated ischemic heart failure: a multicenter, open-label, blinded-outcome, randomized controlled trial.
Phytomedicine
Xianliang Wang, Zhiqiang Zhao, Jingyuan Mao +43 more
Patients with acute decompensated ischemic heart failure (ADIHF) often present with severe clinical symptoms and poor quality of life. In China, Yiqi Fumai lyophilized injection (YQFM) is widely used in the treatment of ADIHF. However, high-quality evidence is still needed to support its efficacy and safety.
Association Analyses Between the NPPB:rs198389 Gene Polymorphism, NT-proBNP Serum Concentrations and Phenotypic Features in Patients with Heart Failure.
Genes (Basel)
Anna Gorący-Rosik, Jakub Rosik, Klaudyna Lewandowska +2 more
Heart failure (HF) is a complex disease and one of the major causes of morbidity and mortality in the world. Increased B-type natriuretic peptide (BNP) levels have been associated with HF. The NPPB:rs198389 (c.-381T > C) promoter polymorphism has been found to modulate BNP levels.
Clinical, Metabolic, and Behavioral Correlates of Nutritional Status in Chronic Heart Failure.
Nutrients
Katarzyna Lomper, Julia Buczkowska
Heart failure (HF) is a chronic condition associated with frequent hospitalizations and impaired quality of life. Malnutrition is common in HF and is linked to adverse clinical outcomes, while self-care is an important component of HF management. This study aimed to examine the associations between nutritional status, self-care behaviors, and clinical characteristics in patients with chronic HF.