Periodontitis, a chronic inflammatory disease, damages the soft tissues and bones around the teeth. Affecting adults, mild periodontitis is common, while severe cases impact up to 20% of individuals, with a prevalence of 45%-50%. This study was aimed at identifying and analyzing the functions of genes differentially expressed in periodontitis through bioinformatics. Additionally, we aimed to validate the causal relationships of these genes with periodontitis using Mendelian randomization.

Intervertebral disc degeneration (IVDD) is a musculoskeletal degenerative disease closely associated with age and immunoreaction. However, the mechanism of senescence and immune infiltration landscape in IVDD is still unclear. Our study was aimed at investigating the pivotal senescence-related genes (SRGs) and immune cells involved in IVDD.

Even though there is strong evidence that exercise improves breast cancer patients' quality of life, treatment tolerance, and survival, disparate research initiatives and uneven clinical acceptance underscore the need for a thorough synthesis of trends, partnerships, and gaps. This bibliometric analysis systematically maps the research landscape of exercise and cardiovascular disease (CVD) from 2020 to 2024, aiming to identify trends, influential works, and knowledge gaps in this critical field. Utilizing data from the Web of Science (WoS) and VOSviewer, the study analyzed 314 articles through cocitation, coword, and co-occurrence analyses. Key findings reveal exponential growth in citations, driven by seminal guidelines (e.g., ESC 2021 and WHO 2020) and studies on sedentary behavior and pandemic-related activity changes. The intellectual structure is anchored by three themes: evidence-based guidelines, risk quantification (e.g., dose-response relationships), and behavioral interventions. Dominant journals include the and , while influential authors like Dominique Hansen and Emmanuel Stamatakis shape the field. Geographic disparities highlight Western-centric research dominance, though emerging contributions from Asia and Europe are noted. The study identifies gaps in mechanistic research, personalized exercise prescriptions, and equitable translation of evidence into practice. Practical implications call for standardized clinical protocols, dual public health messaging (activity promotion and sedentary reduction), and digital health integration. This analysis provides a roadmap for future research, emphasizing transdisciplinary collaboration to optimize CVD prevention through physical activity.

The mechanisms contributing to diabetic vasculopathy have not been fully understand.

Glioma is the most common primary malignant brain tumor, characterized by high mortality and poor prognosis. Disulfidptosis, a recently identified form of regulated cell death, has been implicated in tumor progression; however, its role in glioma remains unclear. In this study, we developed and validated a novel prognostic signature based on disulfidptosis-related long noncoding RNAs (DRLs) by integrating transcriptomic and clinical data from The Cancer Genome Atlas. Seven DRLs were identified to construct a risk model that effectively stratified patients into high- and low-risk groups with significantly different overall survival outcomes. Functional enrichment and immune-related analyses revealed that the high-risk group exhibited distinct immune microenvironment features, including altered immune cell infiltration, immune checkpoint expression, and activity of immune-related pathways, suggesting a potential link between DRLs and immune modulation. Drug sensitivity analysis identified several chemotherapeutic agents and targeted inhibitors with higher predicted efficacy in the high-risk group, offering insights into personalized treatment strategies. In vitro experiments further demonstrated that LINC02542 knockdown significantly suppressed glioma cell proliferation, migration, and invasion. Collectively, these findings indicate that the DRL signature functions as an independent prognostic indicator and a potential biomarker for immune landscape profiling and immunotherapy response prediction in glioma. This integrative multiomics approach provides novel perspectives for precision immunotherapy and targeted therapy in glioma.

Chaperonins are crucial regulators of tumor biology by controlling the stability and function of oncogenic and tumor-suppressor proteins, influencing various tumorigenic signaling pathways. Although chaperonins have been widely discussed in various cancers, including hepatocellular carcinoma (HCC), the complex mechanisms by which they contribute to HCC progression remain insufficiently explored and require further investigation.

The role of sphingolipid metabolism (SM) dysregulation in promoting bladder cancer (BLCA) progression and influencing patient prognosis has been well documented. To enhance therapeutic strategies, we aimed to identify key sphingolipid metabolism-related genes (SMGs) and develop a prognostic signature for personalized BLCA management. In this study, 430 BLCA samples from The Cancer Genome Atlas (TCGA) were analyzed via univariate Cox regression to screen critical SMGs involved in tumor progression. A LASSO regression model was applied to minimize overfitting, followed by multivariable Cox regression to construct and validate a SMG-based prognostic signature in an independent cohort. Key findings revealed that SM dysregulation correlated with poor clinical outcomes and eight pivotal prognostic genes (ATP13A2, PCSK2, NR2F1, GSDMB, NFASC, NTF3, LGALS4, and SREBF1) were identified. The resulting risk model demonstrated robust prognostic performance with AUC values of 0.772 (training cohort) and 0.725 (validation cohort). Notably, high-risk patients exhibited a highly active immunological profile characterized by elevated immune scores and enhanced functionality across 26 immune components, including increased infiltration of NK cells, CD8 T cells, and elevated cytolytic activity. These results suggest that SM dysregulation may drive immunomodulatory changes in BLCA microenvironments, offering mechanistic insights into tumor immune evasion. This study provides a novel biomarker tool for risk stratification and highlights SM pathways as potential therapeutic targets for BLCA patients with immune microenvironment dysregulation.

Acute respiratory distress syndrome (ARDS) is a critical condition characterized by diffuse alveolar damage and intense inflammatory responses. During the COVID-19 pandemic, its incidence and mortality have remained persistently high. Conventional approaches have struggled to uncover the complex cellular heterogeneity and dynamic inflammatory networks underlying ARDS. The advent of single-cell sequencing technologies has revolutionized our ability to dissect the molecular mechanisms of ARDS. This review systematically summarizes recent advances in the application of single-cell sequencing in studying pulmonary inflammation in ARDS, with a focus on its strengths in elucidating immune cell heterogeneity, reconstructing intercellular communication networks, and identifying potential therapeutic targets. Furthermore, we discuss current technical limitations and translational challenges, aiming to provide a theoretical foundation and future direction for translating mechanistic insights into precision medicine for ARDS.

Observational studies have suggested possible links between reproductive factors and bone mineral density (BMD) and osteoporosis (OP), but the causal impact of menstrual factors on BMD remains obscure.

The study is aimed at investigating the functions of P3H4 in liver cancer.

Hyperuricemia (HUA) is a metabolic disorder characterized by elevated serum uric acid (UA) level, which would trigger inflammatory processes contributing to kidney damage. Acupuncture stimulation of BL23, a therapeutic strategy in traditional Chinese medicine (TCM), has been reported to promote diuresis and suppress the immune system and seems to be efficacious in HUA. In this study, we aimed to investigate the effect of electroacupuncture (EA) at BL23 on HUA and HUA-induced kidney inflammation and dysfunction in mice. Mice received EA once daily after being given intragastric potassium oxonate (500 mg/kg) and adenine (100 mg/kg). EA administration not only decreased the levels of serum UA, creatinine, blood urea nitrogen, urinary UA, and protein, along with increased urinary CREA excretion, but also decreased the inflammatory cytokines productions (IL-1, IL-6, and TNF-) in serum. scRNA-seq of treated kidneys revealed that EA at BL23 suppressed the NLRP3 inflammasome complex, the IL-6/JAK/STAT3 signaling pathway, and the production of IL-6 and IL-1 in HUA mice. Western blot analyses verified that EA suppressed the HUA-induced NLRP3 inflammasome activation by promoting autophagy. In conclusion, the study demonstrated that EA at BL23 exhibited anti-HUA and nephroprotective effects by inhibiting both the NLRP3 inflammasome and the IL-6/JAK/STAT3 signaling pathway, reducing renal inflammation and supporting its therapeutic potential for HUA-associated kidney injury.

Keloid is a common pathological scar tissue, which invades the surrounding normal skin and leads to symptoms such as pain, pruritus, erythema, and edema, thereby impacting the quality of life. In this study, we conducted bioinformatics analysis of keloid fibroblasts and normal skin tissue to identify DEGs and the pathways involved in the mechanism of keloid fibroblast proliferation.

The objective of this study is to explore mitochondria-associated programmed cell death (mtPCD)-related key biomarkers for patients with colorectal cancer (CRC).

Chronic obstructive pulmonary disease (COPD), a prevalent chronic respiratory disorder with high morbidity and mortality, is closely associated with mitochondrial dysfunction and immune dysregulation; however, the underlying mechanisms remain unclear.

Osteonecrosis of the femoral head (ONFH) is a challenging global health issue with an unclear pathogenesis, complicating the development of effective treatment strategies. Bone marrow edema (BME) is a critical imaging indicator of ONFH progression, yet its underlying mechanisms remain poorly understood.

The aim of this study is to explore the potential target of Tongmai Xianxiang in the prevention and treatment of postherpetic neuralgia (PHN) by gas chromatography-mass spectrometry (GC-MS) and network pharmacology.

Ageing contributes to the onset of various diseases. It is accompanied by malfunctioning and deterioration of the body systems. Identifying the biomarkers for the prediction, diagnosis, management, or prognosis of ageing and biological ageing was the aim of this study.

This research sought to investigate the impact and underlying mechanisms of growth hormone (GH) on atherosclerosis (AS) based on the analysis of single-cell RNA sequencing (scRNA-seq) data.

Atrial fibrillation (AF) is the most common cardiac arrhythmia, contributing to substantial morbidity, mortality, and healthcare burden. While genome-wide association studies (GWAS) have identified numerous genetic variants linked to AF risk, the causal roles of proteolytic enzymes such as cathepsins remain poorly defined. This study employed bidirectional and multivariable Mendelian randomization (MR) approaches to investigate the causal relationship between genetically determined cathepsin levels and AF risk.

To address the clinical uncertainty surrounding the effect of antihypertensive drugs on dental caries, this study was aimed at investigating the causal relationships between antihypertensive medication use and the risk of dental caries, utilizing a drug-target Mendelian randomization (MR) approach.

Due to the growth in the global consumption of assisted reproductive technology (ART), it is possible that long-term health impacts on offspring have come into focus. ART has offered a welcome solution to infertility, but the fear has been on its effect on the metabolic health of children born on their behalf. Past studies indicate that ART-conceived individuals can have characteristic metabolic profiles relative to their naturally conceived (NC) peers and are therefore potentially predisposed to changes in lipid and glucose handling. Physiopathological glycolipid metabolism, a hallmark of cardiometabolic health, is believed to be modulated not only by environmental and other external factors but also by intracellular regulation proteins, including sterol regulatory element-binding protein (SREBP) and miR-33, although there is little evidence on the effects of ART on these regulatory pathways in early childhood.