Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025081
Resident CD24+LCN2+ liver progenitor cells (LPCs) reportedly contribute to the expanding ductular reaction and macrophage-mediated inflammation associated with chronic liver damage. Both ductular reactions and macrophage-driven inflammation are associated with liver fibrosis and injury in various mouse liver disorders. This study aims to investigate the molecular phenotypes of LPCs and their regulatory mechanisms in humans with non-alcoholic steatohepatitis (NASH). Single-cell RNA sequencing (scRNA-seq) datasets are used to characterize the status and molecular phenotypes of LPCs in clinical NASH samples. To elucidate the regulatory mechanisms of LPCs, CellChat and NicheNet are employed to assess cell-cell communication between LPCs and other cell types. The findings are validated using RNA sequencing datasets associated with NASH progression, NASH mouse models (CDAHFD and HFD), and human NASH liver samples. Results show that resident CD24+LCN2+ LPCs are identified and found to be significantly enriched in NASH patients. Cell communication analyses predict strong interactions between LPCs and proinflammatory macrophage subtypes. Additionally, in NASH, the liver recruits peripheral blood mononuclear cell (PBMC)-derived macrophages and polarizes them into proinflammatory subtypes. The macrophage subtype MP-2 is identified as the primary recipient of LPC-derived signals, exhibiting marked hyperactivation of the NF-κB pathway and a strong association with liver fibrosis. Finally, the MP-2 markers COL10A1 and TPPP3 are characterized and validated. In summary, this study reveals that resident CD24+LCN2+ LPCs are activated in NASH and contribute to fibrosis progression by promoting the activation of the proinflammatory COL10A1+TPPP3+ macrophage subtype.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21700
BACKGROUND: Some patients report dissatisfaction after total knee arthroplasty due to persistent issues like limited mobility, joint instability, and residual pain. To address these challenges, various osteotomy methods and alignment strategies have been proposed and clinically implemented. However, the optimal approach remains debated, with no clear consensus. OBJECTIVE: To comprehensively analyze global trends in alignment techniques for total knee arthroplasty and identify research hotspots through bibliometric and visual analysis, offering evidence-based insights to guide clinical decision-making. METHODS: We retrieved publications (articles and reviews) on total knee arthroplasty alignment techniques published between January 1, 2015 and December 31, 2024, from the Web of Science database (https://www.webofscience.com, developed by the Institute for Scientific Information, USA). Data on countries, institutions, publication years, authors, journals, mean citation rates, H-index, titles, keywords, and the top 25 most-cited articles were extracted and analyzed. VOSviewer and Citespace software were used to analyze keyword co-occurrence and predict research hotspots. RESULTS AND CONCLUSION: A total of 866 publications were identified, including 792 articles and 74 reviews. The United States had the highest number of publications, with the University of California being the most prolific institution and Howell, Stephen M being the most prolific author. The journal 'Knee Surgery Sports Traumatology Arthroscopy' had the highest publication and citation counts. Common keywords included total knee arthroplasty, alignment technique, arthroplasty, clinical outcomes, and survival rate. Keyword and reference burst detection indicated that kinematic alignment and robotic navigation are future research hotspots. The number of publications on total knee arthroplasty alignment techniques is increasing annually. The United States is currently the leading contributor, followed by the United Kingdom. Increasingly precise tools, such as computer-assisted navigation and patient-specific instrumentation, are being developed and applied to achieve alignment goals, but no optimal solution has yet been established. Future research frontiers may include 'robot-assisted navigation', 'patient satisfaction', 'long-term survival', 'indication range', and 'patient-specific alignment'.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025081
Non-alcoholic steatohepatitis (NASH) represents a progressive form of metabolic dysfunction-associated steatotic liver disease with limited therapeutic options. Ductular reactions and macrophage-driven inflammation are associated with liver fibrosis in various chronic liver disorders. This study investigates the molecular phenotypes of resident CD24+LCN2+ liver progenitor cells (LPCs) and their regulatory mechanisms in human NASH. Single-cell RNA sequencing datasets were employed to characterize LPC status in clinical NASH samples. CellChat and NicheNet analyses assessed cell-cell communication between LPCs and other cell types. Findings were validated using RNA sequencing datasets associated with NASH progression, NASH mouse models (CDAHFD and HFD), and human NASH liver samples. Results demonstrate that resident CD24+LCN2+ LPCs are significantly enriched in NASH patients. Cell communication analyses predict strong interactions between LPCs and proinflammatory macrophage subtypes. In NASH, the liver recruits peripheral blood mononuclear cell-derived macrophages and polarizes them into proinflammatory subtypes. The macrophage subtype MP-2 is identified as the primary recipient of LPC-derived signals, exhibiting marked hyperactivation of the NF-κB pathway and strong association with liver fibrosis. The MP-2 markers COL10A1 and TPPP3 are characterized and validated. This study reveals that resident CD24+LCN2+ LPCs are activated in NASH and contribute to fibrosis progression by promoting activation of the proinflammatory COL10A1+TPPP3+ macrophage subtype. These findings delineate a cellular crosstalk axis that may serve as a therapeutic target for NASH fibrosis.