Pectin, a structurally diverse plant-derived polysaccharide, is emerging as a distinctive platform for engineering bioinstructive nanofibrous scaffolds.  Compared to other natural polymers commonly used in electrospinning, such as alginate, hyaluronic acid or collagen, pectin offers a unique combination of mucoadhesiveness, immunomodulatory potential, and fine-tunable molecular architecture governed by the balance of homogalacturonan and rhamnogalacturonan domains. However, its intrinsic polyelectrolyte behavior, low chain entanglement, and high aqueous solubility have historically constrained its use in nanofiber fabrication. Recent advances in chemical modification, solvent engineering, and post-spinning stabilization have enabled the generation of electrospun pectin fibers with controllable morphology, mechanical resilience, and degradation kinetics. This review introduces a predictive structure–property–function framework for the rational design of electrospun pectin nanofibers in biomedical applications. We classify molecular strategies into three groups (covalent, physical, and compositional) and evaluate how each of them affects fiber formation and downstream biological performance, with particular focus on immunological interaction, bioactive loading, and scaffold remodeling. In parallel, we identify translational bottlenecks including material variability, sterilization sensitivity, and regulatory misalignment of crosslinking chemistries. By integrating these factors into a design-informed scaffold logic, this review provides a roadmap for advancing electrospun pectin materials from laboratory prototypes to clinically viable platforms for regenerative medicine, wound healing, and localized therapeutic delivery.

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide, necessitating a deeper understanding of its molecular mechanisms. Extracellular vesicles (EVs) – exosomes, microvesicles, and apoptotic bodies and less-studied subtypes – have emerged as key intercellular communication mediators in cardiovascular diseases. These nanosized particles carry bioactive molecules such as proteins, lipids, and nucleic acids, influencing processes including cardiac remodeling, inflammation, fibrosis, and angiogenesis.

EVs derived from cardiomyocytes, endothelial cells, fibroblasts, and immune cells contribute to HF progression by modulating pathological signaling pathways. For instance, cardiomyocyte-derived EVs may propagate hypertrophy and apoptosis, while fibroblast-derived EVs promote extracellular matrix deposition, leading myocardial stiffness. Conversely, certain EV subpopulations exhibit cardioprotective effects, underscoring their dual role in HF pathogenesis. This review summarizes current knowledge on EV biogenesis, composition, and function in HF, highlighting their diagnostic and therapeutic potential.

We discuss emerging evidence from preclinical and clinical studies, focusing on EV-based biomarkers for early diagnosis and prognosis of HF. Furthermore, we explore therapeutic applications of engineered EVs for targeted drug delivery. Despite considerable advances, unresolved issues such as EV heterogeneity, a lack of standardization isolation methods, and difficulties in applying the results in practice. Addressing these challenges is crucial for unlocking novel strategies for HF management. Integration of fundamental and clinical findings was used to analyze the role of EVs in HF and to evaluate their potential for novel diagnostic and therapeutic applications.

Childhood obesity is associated with chronic low-level inflammation, which is considered a key mechanism in the development of insulin resistance, dyslipidemia and increased cardiovascular risk. Increased levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP) and high-sensitivity CRP (hs-CRP) have been reported in children with obesity, but research results are contradictory, and pooled quantitative estimates of the levels of these biomarkers for the pediatric population have not yet been conducted.

The aim of the study was to systematize data on inflammatory biomarkers in children with obesity and to compare their levels quantitatively with control groups.

A systematic search of publications was conducted in the databases PubMed, Scopus, Web of Science, Semantic Scholar, e-Library and Google Scholar (until August 2025). Observational studies were included in children and adolescents aged 6–18 years with obesity diagnosed according to WHO criteria or national standards, which reported levels of CRP, hs-CRP, IL-6 or TNF-α.

The meta-analysis included 21 studies with a total of 11,193 participants. Children with obesity showed a significant increase elevated levels of all the inflammatory cytokines studied. The most pronounced difference was noted for CRP, g = −1.30 (95% CI: −2.32; −0.29), whereas hs-CRP, g = −0.70 (95% CI: −1.01; −0.39), IL-6, g = −0.51 (95% CI: −0.80; −0.21) and TNF-α, g = −0.60 (95% CI: −0.97; −0.24) demonstrated moderate, but stable and significant effects.

To our knowledge, this is the first meta-analysis to summarize data on inflammatory cytokines in children with obesity. hs-CRP showed a more moderate effect size but more stable and reproducible results which make it suitable for clinical use. Importantly, these findings gain additional significance when viewed in the context of studies in adolescents, adults, and the elderly, where dynamic of inflammatory cytokines are associated with subclinical vascular changes, cardiovascular events, and mortality. Elevated levels of these markers in childhood may serve as an early biological signal of long-term cardiometabolic risk.

The prevalence of temporomandibular joint (TMJ) disorders in the modern world is steadily increasing, and according to the World Health Organization, more than 78% of the working population suffers from muscular and joint disorders. The article reviews the problem of TMJ disorders complex therapy and describes modern treatment methods of TMJ dysfunction.

The detailed description is provided for two approaches to the treatment of TMJ dysfunction: arthrocentesis and splint therapy. We have presented summarized data from clinical studies in which patients were treated for TMJ diseases with hyaluronic acid injections. The main types of occlusal splints and their characteristics, used in the treatment of TMJ dysfunction, are described. We conducted a comparison of both treatment methods for TMJ diseases and identified the key advantages and disadvantages of the reviewed approaches.

Both injection therapy (arthrocentesis) and splint therapy demonstrate high treatment success rates, but each method has its own features in clinical application. Given the high prevalence of TMJ disorders, the issue of developing an improved treatment protocol for these patients remains relevant.

Introduction. Connective tissue dysplasia (CTD) is a hereditary, multifactorial condition characterized by impaired development of connective tissue during the embryonic and postnatal periods. This impairment results from genetically determined defects in the formation, maturation, and metabolism of cells and the extracellular matrix. The aim of this study was to investigate the associations of three polymorphic variants of the ADAMTS5 gene with CTD in general, and with specific phenotypic features of CTD.

Materials and Methods. A cross-sectional study was conducted. The study included 181 participants (35 males, 19.3%, 146 females, 80.7%) with a mean age of 21.9 with a standard deviation of 2.9 years. At the first stage, all participants underwent a clinical examination, and signs of CTD were assessed using the Kadurina T.I. score, as modified by Tyurin A.V. The subsequent stage involved a molecular genetic analysis. Statistical data processing was performed using Excel 2024 and GraphPad Prism 8 software packages.

Results. The clinical examination, utilizing quantitative scoring methods, revealed signs of CTD in 130 subjects (71.8%). A comparative analysis of the allele and genotype frequency distributions for the ADAMTS5 gene loci (rs226794, rs9978597, and rs2830585) revealed the following significant associations: the A allele and AA genotype of rs226794 with the presence of internal organ hernias (p=0.015 and p=0.007, respectively); the T allele and TT genotype of rs9978597 with CTD (p=0.003 and p=0.004, respectively); and the T allele and TT genotype with skin hyperelasticity (p=0.03 and p=0.03, respectively) and hypotension (p=0.015 and p=0.02, respectively).

Conclusion. Thus, the polymorphic variant rs226794 of the ADAMTS5 gene is a risk marker for the development of internal organ hernias, while rs9978597 is a risk marker for CTD, skin hyperelasticity, and hypotension.