Mengyuan Wang

A multifunctional high internal phase Pickering emulsion (HIPPE‐QU) is developed to address immune dysregulation in periodontitis by reprogramming macrophage metabolism and promoting tissue regeneration. Fabricated via one‐step homogenization, HIPPE‐QU features a 75% internal phase and is co‐stabilized by gelatin nanoparticles (GNPs) and copper‐doped hydroxyapatite (HA‐Cu), forming a gel‐like, injectable emulgel suitable for clinical application. Hydrophobic quercetin (QU) is encapsulated in the internal phase and chelates with Cu ² ⁺ and Ca ² ⁺ at the interface, enabling sustained and pH‐responsive release under the acidic periodontal environment. The spatially organized loading strategy across dispersed, interfacial, and internal phases yields synergistic antibacterial and immunoregulatory effects. Mechanistically, HIPPE‐QU modulates macrophage glycolysis and ATP metabolism via HIF‐1 signaling, suppresses ROS overproduction, and promotes M1‐to‐M2 polarization. In vivo, HIPPE‐QU alleviates inflammation, restores BMSC osteogenic capacity, and enhances periodontal tissue regeneration. This work presents an innovative immune‐reprogramming platform with translational potential for precision modulation of the periodontal immune microenvironment.

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Objective: As the global population ages, promoting healthy aging has become increasingly important. Although metabolic syndrome (MetS) is associated with aging, current research evidence remains insufficient.Methods: Data from the 1999–2010 National Health and Nutrition Examination Survey (NHANES) were used for analysis. This dataset includes comprehensive demographic characteristics and biochemical markers. Weighted multivariable logistic regression models were employed to analyze the associations between MetS, its components, and accelerated aging (quantified by PhenoAge Acceleration, PhenoAgeAccel). Restricted cubic spline (RCS) curves were used to explore non-linear relationships between MetS, its components, and PhenoAgeAccel.Results: The study included 10,049 participants, with a mean age of 45.90 years. Compared to participants without MetS, those with MetS showed an increase in age by 0.61 years (β 0.61, 95% CI 0.12–1.10). Among the five components of MetS, after adjusting for all covariates, significant positive associations were observed only for hypertension (β 0.92, 95% CI 0.36–1.48), reduced HDL-C (β 0.66, 95% CI 0.28–1.04), and elevated blood glucose (β 1.43, 95% CI 0.92–1.94).Conclusion: Our study demonstrates that patients with MetS are associated with an increased risk of biological aging, with significant contributions from hypertension, elevated blood glucose levels, and reduced HDL-C to the aging process. These findings provide valuable insights for developing public health strategies to mitigate aging.

Methylation, a key epigenetic modification, is essential for regulating gene expression and protein function without altering the DNA sequence, contributing to various biological processes, including gene transcription, embryonic development, and cellular functions. Methylation encompasses DNA methylation, RNA methylation and histone modification. Recent research indicates that DNA methylation is vital for establishing and maintaining normal brain functions by modulating the high-order structure of DNA. Alterations in the patterns of DNA methylation can exert significant impacts on both gene expression and cellular function, playing a role in the development of numerous diseases, such as neurological disorders, cardiovascular diseases as well as cancer. Our current understanding of the etiology of neurological diseases emphasizes a multifaceted process that includes neurodegenerative, neuroinflammatory, and neurovascular events. Epigenetic modifications, especially DNA methylation, are fundamental in the control of gene expression and are critical in the onset and progression of neurological disorders. Furthermore, we comprehensively overview the role and mechanism of DNA methylation in in various biological processes and gene regulation in neurological diseases. Understanding the mechanisms and dynamics of DNA methylation in neural development can provide valuable insights into human biology and potentially lead to novel therapies for various neurological diseases.

[This corrects the article DOI: 10.3389/fimmu.2024.1258740.].

Ubiquitin-specific proteases (USPs), as one of the deubiquitinating enzymes (DUBs) families, regulate the fate of proteins and signaling pathway transduction by removing ubiquitin chains from the target proteins. USPs are essential for the modulation of a variety of physiological processes, such as DNA repair, cell metabolism and differentiation, epigenetic modulations as well as protein stability. Recently, extensive research has demonstrated that USPs exert a significant impact on innate and adaptive immune reactions, metabolic syndromes, inflammatory disorders, and infection via post-translational modification processes. This review summarizes the important roles of the USPs in the onset and progression of inflammatory diseases, including periodontitis, pneumonia, atherosclerosis, inflammatory bowel disease, sepsis, hepatitis, diabetes, and obesity. Moreover, we highlight a comprehensive overview of the pathogenesis of USPs in these inflammatory diseases as well as post-translational modifications in the inflammatory responses and pave the way for future prospect of targeted therapies in these inflammatory diseases.

Dental mesenchymal stem cells (DMSCs) are crucial in tooth development and periodontal health, and their multipotential differentiation and self-renewal ability play a critical role in tissue engineering and regenerative medicine. Methylation modifications could promote the appropriate biological behavior by postsynthetic modification of DNA or protein and make the organism adapt to developmental and environmental prompts by regulating gene expression without changing the DNA sequence. Methylation modifications involved in DMSC fate include DNA methylation, RNA methylation, and histone modifications, which have been proven to exert a significant effect on the regulation of the fate of DMSCs, such as proliferation, self-renewal, and differentiation potential. Understanding the regulation of methylation modifications on the behavior and the immunoinflammatory responses involved in DMSCs contributes to further study of the mechanism of methylation on tissue regeneration and inflammation. In this review, we briefly summarize the key functions of histone methylation, RNA methylation, and DNA methylation in the differentiation potential and self-renewal of DMSCs as well as the opportunities and challenges for their application in tissue regeneration and disease therapy.