Journal of Hepatology最新文献

{"title":"Erratum to ‘Inhibition of ATGL alleviates MASH via impaired PPARa signalling that favours hydrophilic bile acid composition in mice’ [J Hepatol 82 (2025) 658–675]","authors":"Emmanuel Dauda Dixon , Thierry Claudel , Alexander Daniel Nardo , Alessandra Riva , Claudia Daniela Fuchs , Veronika Mlitz , Georg Busslinger , Hubert Scharnagl , Tatjana Stojakovic , Joana Senéca , Helga Hinteregger , Gernot F. Grabner , Dagmar Kratky , Henkjan Verkade , Robert Zimmermann , Guenter Haemmerle , Michael Trauner","doi":"10.1016/j.jhep.2025.08.003","DOIUrl":"10.1016/j.jhep.2025.08.003","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"83 5","pages":"Page 1236"},"PeriodicalIF":33.0,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144919641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tregs going acid – how cholestasis impairs regulatory T cell function","authors":"Dorothee Schwinge , Christoph Schramm","doi":"10.1016/j.jhep.2025.08.006","DOIUrl":"10.1016/j.jhep.2025.08.006","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"83 5","pages":"Pages 1004-1006"},"PeriodicalIF":33.0,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144916216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcohol activates ATF4/LPLA2-mediated BMP metabolism to enhance HBV-induced hepatocellular carcinogenesis","authors":"Haoxiong Zhou, Junhui Ba, Chuyu Xiao, Huiling Liu, Jie Jiang, Yunwei Guo, Bin Wu","doi":"10.1016/j.jhep.2025.08.022","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.08.022","url":null,"abstract":"<h3>Background &amp; Aim</h3>Chronic alcohol consumption synergistically enhances hepatocellular carcinoma (HCC) risk in hepatitis B virus (HBV)-infected individuals. However, the pivotal molecular mechanisms still remain elusive.<h3>Methods</h3><em>HBx</em>-transgenic (<em>HBx</em>-Tg) mice and nude mouse xenograft models were used to evaluate the tumor-promoting effects of ethanol. Human liver tissues and serum samples, mouse models, HepG2.215 and Hep3B cell lines were further explored to assess the expression and the oncogenic effect of lysosomal phospholipase A2 (LPLA2). Lipid profiles were assessed using liquid chromatography‒mass spectrometry (LC‒MS).<h3>Results</h3>Chronic ethanol intake promoted spontaneous tumorigenesis in <em>HBx</em>-Tg mice and accelerates subcutaneous tumor progression in nude mice. LC‒MS analysis revealed a significant increase in bis(monoacylglycero)phosphate (BMP) species in the tumors of ethanol-fed <em>HBx</em>-Tg mice, which could be attributed to the upregulation of LPLA2. Mechanistic studies revealed that activating transcription factor 4 (ATF4) promoted the transcriptional activity of LPLA2 through direct promoter binding. LPLA2 overexpression promoted tumor cell proliferation <em>in vitro</em> and <em>in vivo</em> by activating the MAPK/ERK signaling pathway, whereas LPLA2 silencing effectively abrogated ethanol-promoted hepatocarcinogenesis. Overexpression of BMP synthase CLN5 and BMP supplementation activated the MAPK/ERK signaling pathway, thereby promoting HCC proliferation. Knockdown of CLN5 counteracted the tumor-promoting proliferation of LPLA2. Clinically, the upregulation of LPLA2 is associated with poor prognosis for HCC.<h3>Conclusion</h3>The data demonstrated that alcohol activates ATF4/LPLA2-mediated BMP metabolism to enhance HBV-induced HCC (HBV-HCC). LPLA2 is a potential therapeutic target and a probable marker of poor prognosis for HCC patients.<h3>Impact and Implications</h3>Chronic alcohol consumption promotes HBV-induced hepatocellular carcinogenesis (HBV-HCC). ATF4/LPLA2-mediated BMP metabolism promotes alcohol-enhanced HBV-HCC via MAPK/ERK signaling pathway. Targeting LPLA2 or BMP metabolism markedly inhibited HBV-HCC progression. This preclinical study provides a theoretical basis to investigate novel strategies for HCC therapy.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"29 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144911192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular Senescence in Liver Diseases: From Molecular Drivers to Therapeutic Targeting","authors":"Kuo Du, David S. Umbaugh, Niansheng Ren, Anna Mae Diehl","doi":"10.1016/j.jhep.2025.08.021","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.08.021","url":null,"abstract":"Obesity, metabolic syndrome, and aging are major contributors to the rising global burden of chronic liver diseases. Among these, aging remains an often underrecognized driver that intersects with other metabolic and environmental insults to exacerbate liver dysfunction. Cellular senescence, a key hallmark of aging, is increasingly implicated as a central mechanism linking these risk factors to liver pathophysiology. Senescent cells accumulate across diverse hepatic cell types and influence disease progression and systemic health through their senescence-associated secretory phenotype (SASP). While senotherapeutic strategies, including senolytics and senomorphics, show promise, their efficacy and safety remain highly dependent on cell type, disease context, and agent specificity. Recent advances, such as multi-omics profiling, multi-marker gene signatures, and targeted modalities including PROTACs and CAR-T cell therapies, offer new opportunities for precision interventions. This review synthesizes emerging insights into the molecular mechanisms of liver senescence, evaluates the current landscape of senotherapies, and outlines key challenges and future directions for safely and effectively targeting senescence in chronic liver disease.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"34 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engineered monoclonal antibody tobevibart enhances HBsAg capture by Fc receptor-positive cells and activates HBV-specific T cells","authors":"Lucia Vincenzetti, Rachel Wong, Roberta Marzi, Barbara Guarino, Erin Stefanutti, Sneha V. Gupta, Laura E. Rosen, David M. Belnap, Li Wang, Yi-Pei Chen, Julia di Iulio, Amin Momin, Karen E. Tracy, Sharvari Deshpande, John M. Errico, Federico Giovannoni, Nicole Sprugasci, Alessia Peter, Lillian Seu, Daniel Cloutier, Michael A. Schmid","doi":"10.1016/j.jhep.2025.08.016","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.08.016","url":null,"abstract":"<h3>Background &amp; Aims</h3>Effective immune targeting is likely essential for achieving functional cure of chronic hepatitis B (CHB). Tobevibart, a human monoclonal antibody against hepatitis B virus (HBV) surface antigen (HBsAg), neutralizes HBV and hepatitis delta virus (HDV). This study aimed to characterize effects of the engineered GAALIE Fc of tobevibart on HBV immune responses.<h3>Methods</h3>We studied tobevibart and its equivalent HBC34*-GAALIE <em>in vitro</em> using electron microscopy, reporter cells, and primary human or mouse immune cells to assess dynamics of HBsAg reduction, dendritic cell (DC) activation, and T cell stimulation. Tobevibart-mediated binding of HBsAg to immune cells was evaluated also in a phase 1 clinical trial in patients with CHB.<h3>Results</h3>The GAALIE Fc of tobevibart increased binding to activating FcγRs, decreased binding to inhibitory FcγRIIb, mediated gain of function in FcγR signaling in immune complexes (ICs) with HBsAg, and increased binding of HBsAg to neutrophils and monocytes <em>in vitro</em> compared to wild-type (WT) Fc. Similarly, administration of 300 mg tobevibart in patients with CHB resulted in binding of HBsAg to these cells in vivo, concurrent with a reduction in circulating HBsAg. <em>In vitro</em>, ICs of HBC34*-GAALIE and HBsAg activated human DCs significantly more than HBC34*-WT. These DCs presented antigen and stimulated HBsAg-specific human T cells. Similarly, HBC34*-GAALIE augmented HBsAg-specific CD4+ T cell responses from mice transgenic for human FcγRs.<h3>Conclusions</h3>We demonstrate that tobevibart combines the advantages of potent neutralization of HBV and HDV with FcγR-mediated reduction of HBsAg and enhancement of T cell responses. Tobevibart is under clinical investigation alone or in combination with other agents to treat patients with chronic hepatitis delta and to induce functional cure of patients with CHB.<h3>Impact and Implications (Lay Summary)</h3>Chronic infection with hepatitis B virus (HBV) or co-infection with hepatitis delta virus (HDV) can cause severe liver disease and cancer. We previously showed that the monoclonal antibody tobevibart potently neutralizes HBV and HDV. Here we demonstrate that the engineered Fc region of tobevibart effectively interacted with several immune cell types, potentially facilitating the rapid removal of damaging viral proteins from circulation and activating T cell responses that may control HBV infection long term.<h3>Clinical trial</h3>VIR-3434-1002, phase 1, <span><span>ClinicalTrials.gov</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> identifier NCT04423393","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"13 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Healthy eating and physical activity significantly lower sex-specific alcohol-attributable liver mortality in the United States","authors":"Eduardo Vilar-Gomez, Lauren Nephew, Samer Gawrieh, Raj Vuppalanchi, Carla Kettler, Francis Pike, Wanzhu Tu, Niharika Samala, Suthat Liangpunsakul, Naga Chalasani","doi":"10.1016/j.jhep.2025.06.033","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.06.033","url":null,"abstract":"<h3>Background &amp; Aims</h3>The impact of diet quality (DQ) and physical activity (PA) on alcohol-related liver mortality is under-researched. This study investigates how DQ and PA influence alcohol-attributable liver mortality in the US.<h3>Method</h3>Data from 60,334 adults in the National Health and Nutrition Examination Surveys (1984-2018) were analyzed and linked to the National Death Index through December 31, 2019. Self-reported alcohol use, DQ (healthy eating index [HEI]), and PA levels were obtained. Participants were classified as light, moderate, or heavy drinkers based on NIAAA guidelines. Physically active participants reported at least 150 min of moderate-intensity PA, 75 min of vigorous-intensity PA, or a combination per week. A healthier diet was defined as being in the top quartile of HEI. The outcome was liver-related mortality.<h3>Results</h3>During a 12.2-year follow-up, 252 liver-specific deaths were recorded. The average daily alcohol intake increased liver-specific mortality risk (adjusted subdistribution hazard ratio [aSHR]-men: 1.04, 95% CI 1.01-1.06; women: 1.08, 95% CI 1.04-1.12) compared to abstainers. Binge drinking also raised liver mortality risk (aSHR-men: 1.52, 95% CI 1.04-2.29; women: 2.52, 95% CI 1.44-4.41) compared to non-binge drinking. Healthier dietary intake (top quartile of HEI) reduced liver mortality risk among non-heavy (aSHR: 0.35, 95% CI 0.13-0.90), heavy (aSHR: 0.14, 95% CI 0.04-0.82), and binge (aSHR: 0.16, 95% CI 0.06-0.46) drinkers compared to unhealthier diets (lower quartile of HEI). Physically active participants had lower liver mortality risk among non-heavy (aSHR: 0.52, 95% CI 0.28-0.94), heavy (aSHR: 0.64, 95% CI 0.35-0.99), and binge (aSHR: 0.31, 95% CI 0.10-0.88) drinkers. Diets high in vegetables, fruits, whole grains, seafood, plant-based proteins, and unsaturated fats – and low in solid fats, alcohol, and added sugars – were protective. The survival benefits of DQ and PA were substantially greater in women than in men.<h3>Conclusion</h3>Healthy eating and increased levels of PA significantly lower the risk of alcohol-attributable liver-related mortality in the US population.<h3>Impact and implications</h3>This study found that any amount of alcohol intake and binge drinking were associated with an increased risk of liver-related mortality. Adherence to healthy dietary patterns and increased physical activity lower the risk of liver mortality across all drinking patterns, including heavy and binge drinking. Liver survival benefits from both physical activity and diet quality are greater in women than men. A diet rich in vegetables, fruits, grains, seafood, plant-based proteins, and unsaturated fatty acids, combined with a reduced intake of empty calories from solid fats, alcohol, and added sugars, is associated with a lower risk of liver-related mortality. Economically disadvantaged populations are exposed to high-risk alcohol use, unhealthy diet, and physical inactivity, and therefore","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"1 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to: “Non-acute decompensation: Ready for clinical practice?”","authors":"Nipun Verma ,&nbsp;Parminder Kaur ,&nbsp;Rajiv Jalan","doi":"10.1016/j.jhep.2025.08.019","DOIUrl":"10.1016/j.jhep.2025.08.019","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"83 5","pages":"Pages e255-e257"},"PeriodicalIF":33.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New targets and new drugs for hepatobiliary cancers","authors":"Stephen L. Chan, Angela Lamarca, Chiun Hsu, Victor Moreno, Landon L. Chan, Bridget P. Keenan","doi":"10.1016/j.jhep.2025.08.018","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.08.018","url":null,"abstract":"The treatment of hepatobiliary cancers has advanced rapidly, with novel approaches and targets under active development. There are two primary directions of drug development based on their mechanisms. The first focuses on novel therapies targeting the immune system beyond conventional immune checkpoints like Programmed death-1 and Cytotoxic T-lymphocyte-associated protein 4. This includes antibodies targeting new immune checkpoints and cytokines involved in tumour immune response regulation. Phase II and III clinical trials are exploring combinations of these antibodies with approved immunotherapy regimens. Cellular therapies, including chimeric antigen receptor-T cells and tumour-infiltrating lymphocytes, are also being tested in early clinical studies for hepatocellular carcinoma (HCC) and biliary tract cancer (BTC). Advances in bispecific antibodies have enabled the design of bispecific T cell engagers. The second direction addresses new targets or revised approaches to traditionally undruggable targets such as Peroxisome proliferator-activated receptors-alpha, Kirsten rat sarcoma viral oncogene, histone deacetylase, and β-catenin. Successful in other cancers, antibody-drug conjugates are also being developed for BTC expressing human epidermal growth factor receptor-2 or nectin-4. Notably, the classification of these advances is somewhat arbitrary, as emerging evidence reveals new immunomodulatory roles for these therapies. Finally, these therapeutic advances suggest a change in the treatment approach for less common liver cancers, such as sarcomatoid HCC and combined HCC-cholangiocarcinoma. Recent clinical experiences and genomic data indicate potential responsiveness to immune checkpoint inhibitors. Including these tumours in clinical trials could facilitate developing treatments for these rare subtypes.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"50 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Hypertension on Long-term Adverse Clinical Outcomes and Liver Fibrosis Progression in MASLD","authors":"Xiao-Dong Zhou, Liyou Lian, Qin-Fen Chen, Seung Up Kim, Terry Cheuk-Fung Yip, Salvatore Petta, Atsushi Nakajima, Emmanuel Tsochatzis, Junping Shi, Wah-Kheong Chan, Jérôme Boursier, Elisabetta Bugianesi, Yusuf Yilmaz, Hannes Hagström, Manuel Romero-Gomez, Khalid Alswat, José Luis Calleja, Hirokazu Takahashi, Victor de Lédinghen, , Ming-Hua Zheng","doi":"10.1016/j.jhep.2025.08.017","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.08.017","url":null,"abstract":"<h3>Background &amp; Aims</h3>Hypertension is common in metabolic dysfunction-associated steatotic liver disease (MASLD), but its impact on long-term clinical outcomes and disease progression remains unclear. This study investigated the association of hypertension and risk of adverse clinical outcomes and progression of liver stiffness/fibrosis in MASLD.<h3>Methods</h3>Three multicenter prospective cohorts were analyzed: the UK BioBank (UKBB) cohort to assess the risk of adverse clinical outcomes, the VCTE-Prognosis cohort to assess liver stiffness/fibrosis progression, and the Paired Liver Biopsy cohort to assess histologic liver fibrosis progression. Adverse clinical outcomes were defined as all-cause mortality, cardiovascular events, and/or liver-related events. Liver stiffness progression was defined as an increase in liver stiffness measurement (LSM) from &lt;10 kPa to ≥10 kPa or an increase of ≥20% for baseline LSM ≥10 kPa. Liver fibrosis progression was defined as a 1-stage fibrosis stage increase. Cox regression and Kaplan-Meier analyses were used to evaluate the impact of baseline hypertension on the outcomes.<h3>Results</h3>107,316 adults from the UKBB cohort, 8,169 from the VCTE-Prognosis cohort, and 1,670 from the Paired Liver Biopsy cohort were included. Hypertension rates were 37.1%, 33.4%, and 48.9%, respectively. In the UKBB cohort, hypertension was associated with long-term adverse clinical outcomes (adjusted HR=1.30, 95%CI 1.26-1.33, P&lt;0.001). In the VCTE-Prognosis cohort, hypertension was associated with a higher risk of liver stiffness progression (adjusted HR=1.57, 95%CI 1.30-1.90, P&lt;0.001), while in the Paired Liver Biopsy cohort, hypertension was associated with a greater risk of histologic liver fibrosis progression (adjusted HR=1.41, 95%CI 1.12-1.78, P=0.004). Subgroup and sensitivity analyses supported these findings.<h3>Conclusions</h3>Hypertension is a modifiable risk factor and increases risk of adverse clinical outcomes and progression of liver stiffness/fibrosis.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"52 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"T Cells in a Drop: Rapid T Cell Monitoring in Chronic Hepatitis B","authors":"Maike Hofmann, Barbara Rehermann","doi":"10.1016/j.jhep.2025.08.008","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.08.008","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Authors’ contributions</h2>M.H. and B.R. conceptualized and wrote the manuscript.</section></section><section><section><h2>Financial Support</h2>M.H. was supported by the Heisenberg program of the German Research Foundation (project no. HO 5836/2-1).</section></section><section><section><h2>Declaration of Competing Interest</h2>The authors declare that they do not have any conflict of interest. Please refer to the accompanying ICMJE disclosure forms for further details.Dr. Rehermann contributed to this article in her personal capacity. The views expressed are her own and do not necessarily represent the views of the National Institutes of Health or the United States Government.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"8 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}