Ozone pollution is a major environmental concern. According to recent epidemiological studies, ozone exposure increases the risk of metabolic liver disease. However, studies on the mechanisms underlying the effects of ozone exposure on hepatic oxidative damage, lipid synthesis, and catabolism are limited. In this study, Huh-7 human hepatocellular carcinoma cells were randomly divided into five groups and exposed to 200 ppb O₃ for 0, 1, 2, 4, and 8 h. We measured the levels of oxidative stress and analyzed the changes in molecules related to lipid metabolism. The levels of oxidative stress were found to be significantly elevated in Huh-7 hepatocellular carcinoma cells after O₃ exposure. Moreover, the expression levels of intracellular lipid synthases, including SREBP1, FASN, SCD1, and ACC1, were enhanced. Lipolytic enzymes, including ATGL and HSL, and the mitochondrial fatty acid oxidase, CPT1α, were inhibited after O₃ exposure. In addition, short O₃ exposure enhanced the expression of the intracellular peroxisomal fatty acid β-oxidase, ACOX1; however, its expression decreased adaptively with longer exposure times. Overall, O₃ exposure induces an increase in intracellular oxidative stress and disrupts the normal metabolism of lipids in hepatocytes, leading to intracellular lipid accumulation.

Osteoporosis (OP), a prevalent disease among middle-aged and elderly individuals, is characterized by a decrease in bone mineral density (BMD), which predisposes individuals to fragile fractures. The core pathological process involves excessive bone resorption over bone formation. The etiology of OP is intricate, and increasing recent studies have focused on the role of gut microbiota (GM) in its pathogenesis. Harmful bacteria exacerbate OP, whereas probiotics are beneficial for bone metabolism and delay the progression of OP. GM influences the progression of OP through various mechanisms, including the production of metabolites, modulation of the intestinal barrier, and regulation of intestinal immunity and osteoimmunology. In this review, we summarize the role of GM in the pathogenesis of OP based on the latest understandings, and highlight the promising potential of strategies targeting GM for the intervention and management of OP.

Background: Receptor activator of nuclear factor kappa-B ligand (RANKL) plays a critical role in bone metabolism and the pathogenesis of osteoporotic fractures. This study aims to conduct a bibliometric analysis of global research pertaining to RANKL and osteoporotic fractures to identify key trends, influential studies, and collaborative networks.Methods: A literature search was conducted to identify articles found in the Web of Science Core Collection database regarding RANKL and osteoporotic fractures from 2001 to 2024. A bibliometric analysis was performed using VOSviewer, CiteSpace, and R 4.3.3 for the publication volume, country and institution contributions, journal impact, author influence, and research hotspots.Results: A total of 214 articles were analyzed. Publication rates have steadily increased, with a peak of 21 papers in 2020. The U.S., China, and South Korea were the top contributing countries, and leading institutions included Harvard University and Dankook University. The Journal of Bone and Mineral Research, Osteoporosis International, and Bone were the journals of highest impact. At the level of authors, Heiss–Christian published the highest number and Christiansen–Claus had the strongest citation impact (1,368 citations). Research evolved from basic biological mechanisms (2001–2010) through clinical applications (2011–2017) to recent renewed interest in fundamental RANKL biology (2018–2024). Key research hotspots included postmenopausal osteoporosis, bone mineral density, and osteoclast differentiation, with emerging focus on RANKL’s role beyond skeletal metabolism.Conclusion: This bibliometric analysis provides a comprehensive overview of RANKL research in osteoporotic fractures, highlighting key priorities for future investigation. Future studies should prioritize understanding RANKL’s broader physiological roles, developing better predictive markers, and optimizing personalized treatment strategies.

Periprosthetic joint infection (PJI) poses significant challenges to arthroplasty outcomes, necessitating translational animal models for pathogenesis studies and therapeutic development. This study aimed to establish a standardized Beagle PJI model by integrating species-specific 3D-printed femoral prostheses with quantitative bacterial inoculation, while evaluating the dose-dependent effects of Staphylococcus aureus (S. aureus) on infection progression. Two titanium alloy prostheses were designed using CT-based anatomical data: BFP-C (canine-optimized) and BFP-H (human-derived). Prostheses underwent mechanical compression tests, finite element analysis (FEA) simulating postoperative and osseointegration phases, and in vivo validation in Beagles. The optimized BFP-C was selected for PJI model construction via hemi-hip arthroplasty (HHA), with intraoperative inoculation of S. aureus ranging from 250 to 10^8 colony-forming units (CFU). Longitudinal evaluation included radiography (X-ray/CT), mechanical pull-out tests, histopathology (H&E/Masson/Giemsa staining), bacterial cultures, and mobility assessments using open-field behavioural tracking. BFP-C exhibited superior biomechanical compatibility, with 12.3-fold higher yield strength (6836 ± 157 N vs. 553 ± 49 N) and 97 % reduction in bone strain (0.71 % vs. 20.32 %) compared to BFP-H. All inoculated groups developed PJI with dose-dependent severity: ultra-high-dose (10^8 CFU) groups displayed severe osteolysis (pull-out strength: 24 ± 8 N vs. 924 ± 45 N in controls), biofilm formation, and mobility impairment (74 % reduction in distance travelled, 2003 ± 276 cm vs. 7976 ± 333 cm in controls), whereas low-dose (250 CFU) groups established PJI with milder manifestations, evidenced by sinus tract formation, 55.1 % reduction in pull-out strength (406 ± 15 N vs. 924 ± 45 N in controls), and concordant radiological/histopathological signs of infection. Imaging examinations revealed differential osteolytic patterns corresponding to bacterial loads. Combined wound evaluation and microbiological analyses confirmed consistent infection establishment across all replicates. This Beagle PJI model successfully recapitulates clinical infection dynamics, emphasizing the critical role of species-specific prosthesis design and standardized bacterial quantification. The integrated multimodal evaluation system (imaging, biomechanical, and behavioural analyses) demonstrated both the reliability of the model and its sensitivity in detecting infection progression. Its modular design supports customization for studying biofilm-resistant implants or antibiotic delivery systems. These findings not only provide a critical tool for mechanistic PJI research but also establish a theoretical foundation for clinical translation, with the quantitative multimodal framework directly informing diagnostic and therapeutic strategies. Beyond serving as a preclinical platform for anti-infective therapies, the model provides actionable insights into optimizing human prosthetic biomechanics, such as reducing stress shielding through FEA-informed design principles. The 3D printing workflow further demonstrates rapid prototyping capabilities for patient-specific orthopaedic implants.

Osteoarthritis (OA) is a prevalent cause of joint pain in elderly individuals, and chondrocyte senescence plays a crucial role in its pathogenesis. FOXO4 has been identified as a crucial molecule in cellular senescence. However, little is known regarding its role in OA and the regulation of its expression. 17‐β‐Estradiol (E2) has been demonstrated to exert a protective effect in OA, yet the underlying mechanism remains largely unexplained. In this study, we reported a protective effect of E2 against multiple types of chondrocyte senescence, and this effect was mediated by oestrogen receptor α (ERα). Mechanically, E2 activated AKT and facilitated the nuclear export and the degradation of FOXO4, which played a crucial role in resisting senescence. Moreover, knockdown of FOXO4 in osteoarthritic chondrocytes alleviated cellular senescence. Furthermore, we demonstrated that intra‐articular injection of E2 was effective in ameliorating surgery‐induced OA in a rat model. Collectively, E2 contributed to the alleviation of chondrocyte senescence through the ERα‐AKT‐FOXO4 signalling pathway and ameliorated OA progression in the rat model. Our study offers a novel therapeutic approach for controlling chondrocyte senescence and provides insights into the role of E2 in treating OA.

Sarcopenia is a disease characterized by reduced muscle mass and strength. In recent years, increasing evidence suggests that gut microbiota (GM) may play an important role in the pathogenesis of sarcopenia. GM is associated with muscle health by affecting muscle metabolism, regulating inflammatory responses, and promoting nutrient absorption. Despite recent rapid research progress, there are still many uncertainties regarding the causal relationship between GM and sarcopenia, key effector molecules, and individualized intervention strategies. We review the mechanisms of GM in the pathogenesis of sarcopenia with a focus on four interconnected pathways: chronic inflammation, nutrient absorption, amino acid metabolism, and GM-derived metabolites. This review aims to propose an integrated framework linking GM to muscle homeostasis to guide future research directions. Interventions targeting GM may offer a new approach for the treatment of sarcopenia, but more research is needed to clarify the causal relationship and optimize intervention measures.