Articular cartilage injury represents a significant clinical challenge, with traditional treatments providing limited efficacy. Advances in regenerative medicine and digital education have created new opportunities for both cartilage repair therapies and innovations in medical education. This study aims to systematically analyze the research status, hotspots, and development trends in these two fields from 2013 to 2024 using bibliometric and visualization methods. Literature was retrieved from the PubMed, Embase, and Scopus databases for English articles published between 1 January 2013 and 1 December 2024. A search strategy combining medical subject headings (MeSH) and free-text keywords was employed, resulting in 5,589 included articles. CiteSpace 5.8.R3 was used for keyword co-occurrence, co-citation, collaboration network, and burst detection analyses, with time slicing to reveal dynamic trends. Annual publications in cartilage repair treatment showed steady growth, with research hotspots focusing on stem cell therapy, tissue engineering, 3D printing, and biomaterials. In medical education innovation, research concentrated on educational reform, virtual learning, and flipped classrooms. The collaboration network analysis indicated that the United States and Germany played central roles in cartilage repair, while the United States and the Netherlands were central in medical education innovation. Burst keyword analysis revealed a shift in cartilage repair toward personalized therapies and bioprinting, and in medical education toward virtual reality (VR) and blended learning models. The study found that cartilage repair research was moving toward interdisciplinary integration, with personalized and intelligent repair serving as its main development directions. Medical education, leveraging VR and augmented reality technologies, promoted the reconstruction of teaching scenarios and the optimization of learning pathways. Future research should enhance clinical translation, integrate educational technologies, and foster cross-institutional collaboration to promote synergistic innovation in both fields.

Aberrant increases in osteoclast formation and/or activity are the underlying cause of bone loss in a variety of osteolytic diseases. Fatty acid synthase (Fasn)-mediated de novo lipogenesis (DNL) is one of the major lipid metabolic pathways and has been shown to play critical roles in diverse physiological and pathological processes. However, little is known about its role in osteoclastogenesis. Here, we investigate the direct role of DNL in osteoclastogenesis and its therapeutic potential in osteolytic diseases. We found that Fasn expression and DNL levels are upregulated during receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. Inhibition of Fasn by shRNA knockdown or its pharmacological inhibitors (ASC40 and trans-C75) impairs osteoclast differentiation in vitro. Mechanistically, pharmacological inhibition of Fasn suppresses RANKL-induced c-Fos/NFATc1 expression and thus osteoclastogenesis partly by disrupting STAT3 palmitoylation, while promoting ROS scavenging to impair mitogen-activated protein kinase (MAPK) signaling. Finally, the therapeutic potential of ASC40 for the treatment of osteolytic bone loss is tested in two mouse models of osteolytic diseases, i.e. ovariectomy (OVX)-induced osteoporosis and titanium nanoparticle-induced calvarial osteolysis. The results show that ASC40 significantly attenuates bone loss and osteoclastogenesis in both models. In conclusion, our results demonstrate that Fasn-mediated DNL is a novel positive regulator of osteoclastogenesis and may serve as a promising therapeutic target for the treatment of osteoclast-driven osteolytic bone diseases.

Statistical Power of Association With FDR < 0.1 in Subgroup Analysis

The human skeleton is a multifunctional organ made up of multiple cell types working in concert to maintain bone and mineral homeostasis and to perform critical mechanical and endocrine functions. From the beginning steps of chondrogenesis that prefigures most of the skeleton, to the rapid bone accrual during skeletal growth, followed by bone remodeling of the mature skeleton, cell differentiation is integral to skeletal health. While growth factors and nuclear proteins that influence skeletal cell differentiation have been extensively studied, the role of cellular metabolism is just beginning to be uncovered. Besides energy production, metabolic pathways have been shown to exert epigenetic regulation via key metabolites to influence cell fate in both cancerous and normal tissues. In this review, we will assess the role of growth factors and transcription factors in reprogramming cellular metabolism to meet the energetic and biosynthetic needs of chondrocytes, osteoblasts, or osteoclasts. We will also summarize the emerging evidence linking metabolic changes to epigenetic modifications during skeletal cell differentiation.

Description of Hematological Traits Evaluated in This MR Analysis

Causal effects of identified traits considering smoking and bilirubin. (a) Causal effects of 3 identified hematological traits and lung cancer in ever/never smokers. RAPS: Robust Adjusted Profile Score. (b) Effects of 3 identified hematological traits after adjustment for smoking. (c) Effects of 3 identified hematological traits after adjustment for bilirubin level.

Retraction of 'Strontium-doped gelatin scaffolds promote M2 macrophage switch and angiogenesis through modulating the polarization of neutrophils' by Tao Li et al., Biomater. Sci., 2021, 9, 2931-2946, https://doi.org/10.1039/D0BM02126A.

Leave-one-out plot for reticulocyte count on lung carcinoma.

Causal Effects of Identified Traits in Lung Cancer in Ever/Never Smokers Estimated via Seven Methods for Each Association

Retraction of ‘Strontium-doped gelatin scaffolds promote M2 macrophage switch and angiogenesis through modulating the polarization of neutrophils’ by Tao Li et al. , Biomater. Sci. , 2021, 9 , 2931–2946, https://doi.org/10.1039/D0BM02126A.

Causal Effects Estimated via Seven Methods for Each Association

Heterogeneity Test and Pleiotropy Test for Identified Associations

Summary of F Statistic and Variance Explained of Each Hematological Trait

Instrument Variants for Each Hematological Trait

Leave-one-out plot for hematocrit on lung carcinoma.

AbstractBackground: Observational studies have suggested blood cell counts may act as predictors of cancer. It is not known whether these hematologic traits are causally associated with lung cancer. Methods: Two-sample bidirectional univariable Mendelian randomization (MR) and multivariable MR (MVMR) were performed to investigate the causal association between hematologic traits and the overall risk of lung cancer and three histologic subtypes [lung adenocarcinoma, squamous cell lung cancer, and small cell lung cancer (SCLC)]. The instrumental variables of 23 hematologic traits were strictly selected from large-scale genome-wide association studies. Inverse-variance weighted method and five extra methods were used to obtain robust causal estimates. Results: We found evidence that genetically influenced higher hematocrit [OR, 0.845; 95% confidence interval (CI), 0.783–0.913; P = 1.68 × 10−5] and hemoglobin concentration (OR, 0.868; 95% CI, 0.804–0.938; P = 3.20 × 10−4) and reticulocyte count (OR, 0.923; 95% CI, 0.872–0.976; P = 5.19 × 10−3) decreased lung carcinoma risk, especially in ever smokers. MVMR further identified hematocrit independently of smoking as an independent predictor. Subgroup analysis showed that a higher plateletcrit level increased the risk of small cell lung carcinoma (OR, 1.288; 95% CI, 1.126–1.474; P = 2.25 × 10−4). Conclusions: Genetically driven higher levels of reticulocyte count and hematocrit decreased lung cancer risk. Higher plateletcrit had an adverse effect on SCLC. Hematologic traits may act as low-cost factors for lung cancer risk stratification. Impact: Further studies are required to elucidate the potential mechanisms underlying the dysregulation of homeostasis related to hematologic traits, such as subclinical inflammation.

Statistical Power of Identified Association Calculated With mRnd

Introduction: Recent studies have suggested that cartilage progenitor cells (CPCs) could be activated and differentiated into chondrocytes to produce matrix and to restore the integrity of damaged cartilage after injury. However, the mechanism involved in CPC activation upon damage is still unclear. This study aims to investigate the role of high mobility group box chromosomal protein 1 (HMGB1) in both activation and migration of CPCs during cartilage injury.Material and methods: Explants harvested from mature bovine stifle joints were used for impact injury. The proliferation and migration of CPCs were examined via confocal imaging. Gene and protein expression of Hmbg1, Cxcl12, and Cxcr4 was also examined by quantita- tive polymerase chain reaction (qPCR), ELISA, and western blot. Each experiment was repeated 3 times. ANOVA and Student's t-test were performed for statistical analysis.Results: HMGB1 released from dead and damaged chondrocytes after an impact injury could activate CPCs in the superficial zone of cartilage and promote their migration and proliferation to injury sites. However, the block of HMGB1 activation with its specific bind- ing inhibitor glycyrrhizin inhibits the proliferation and migration of CPCs. Further investigations demonstrate that HMGB1 promotes CPCs migration through the pathway of C-X-C motif chemokine 12 (CXCL12) and its receptor CXCR4. Quantitative analysis of HMGB1 in cell culture medium also indicates that CPCs may have a self-activation property after the HMGB1 released from dead cells has been exhausted.Conclusion: HMGB1 is a pivotal factor that could enhance the migration and proliferation of CPCs through the CXCL12/CXCR4 pathway after cartilage injury, which could provide useful information for cartilage repair and osteoarthritis treatment.

Background Mitochondrial dysfunction and aberrant structure in adipose tissue occur in obesity and obesity-linked brown adipose tissue (BAT) whitening; however, whether this aberrant architecture contributes to or is the result of obesity is unknown. Apolipoprotein O (APOO) is a constitutive protein of the mitochondrial cristae organizing system complex. This study aimed to characterize the physiological consequences of APOO deficiency in vivo. Methods APOO expression was analyzed in different human and murine adipose depots, and mice lacking APOO in adipocytes (ApooACKO) are developed to examine the metabolic consequences of adipocyte-specific APOO ablation in vitro and in vivo. Results Results showed that APOO expression is reduced in BAT from both diet-induced and leptin-deficient obese mice. APOO-knockout mice showed increased adiposity, BAT dysfunction and whitening, reduced non-shivering thermogenesis, and blunted responses to cold stimuli. APOO deficiency disrupted mitochondrial structure in brown adipocytes and impaired oxidative phosphorylation, thereby inducing a shift from oxidative to glycolytic metabolism, increasing lipogenic enzyme levels and BAT whitening. APOO inactivation inhibited thermogenesis in BAT by reducing mitochondrial long-chain fatty acid oxidation. It also disturbed peroxisomal biogenesis and very long-chain fatty acid oxidation via peroxisome proliferator-activated receptor α. Conclusions Altogether, APOO deficiency in adipocytes aggravates BAT whitening and diet-induced obesity; thus, APOO could be a therapeutic target for obesity.