Chinese Medical Journal最新文献

{"title":"Improved diagnostic capability, rather than biologics, reduces surgical rates in Chinese Crohn's disease patients: A multicenter study.","authors":"Jian Wan, Zhuo Wang, Jun Shen, Jie Zhong, Naizhong Hu, Lanxiang Zhu, Yinglei Miao, Wensong Ge, Zhonghui Wen, Yufang Wang, Jiaming Zhou, Yong Lyu, Jie Liang, Kaichun Wu","doi":"10.1097/CM9.0000000000004315","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004315","url":null,"abstract":"<p><strong>Background: </strong>Surgical rates for Crohn's disease (CD) are declining globally. However, the driving factors remain unclear, particularly in newly industrialized countries. We aimed to evaluate the impact of diagnostic capacity and treatment with biologics on surgical rates among Chinese CD patients.</p><p><strong>Methods: </strong>Data of CD patients from January 2000 to January 2024 were extracted from 8 sites of the Chinese database for inflammatory bowel disease. Trends in cross-sectional imaging use, surgically diagnosed proportion, medical treatment, and surgery for CD were described. Cumulative surgical rates were compared using Kaplan-Meier method with log-rank test. Time-dependent Cox models were used to identify factors associated with surgery risk, and propensity score matching (PSM) was applied to validate the findings.</p><p><strong>Results: </strong>In total, 1354 patients were included, with a median follow-up of 5.99 years. The cumulative 5-year surgical rate decreased from 30.96% in 2000-2012 to 21.57% in 2013-2024 (log-rank P <0.001). The use of cross-sectional imaging increased from 2.00% in 2000-2004 to 82.81% in 2020-2024. The proportion of surgically diagnosed patients declined from 13.68% in 2000-2012 to 6.21% in 2013-2024. Multivariate Cox analysis showed that diagnosis in 2013-2024 (hazard ratio [HR] 0.74, 95% confidence interval [CI]: 0.59-0.91, P = 0.006) was independently associated with a lower risk of surgery, whereas biologic use (HR 0.93, 95% CI: 0.71-1.22, P = 0.604) was not. Sensitivity analyses excluding surgically diagnosed patients demonstrated similar surgical rates between the two cohorts. PSM and subgroup analyses confirmed these trends.</p><p><strong>Conclusions: </strong>Surgical rates among Chinese CD patients have significantly decreased over the past two decades, in parallel with improvements in diagnosis. Enhancements in diagnostic pathways within broader systemic healthcare upgrades are strongly associated with reduced surgical risk, whereas increased use of biologics is not.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-11 drives Treg cell differentiation by activating the MBD3/APOH-mediated fatty acid oxidation axis to promote hepatocellular carcinoma.","authors":"Yang Gao, Xijuan Yao, Xing Huang, Lian Wang, Yong Wang, Guangyu Zhu, Zhen Wang, Lu Li, Jinhe Guo, Jian Lu","doi":"10.1097/CM9.0000000000004371","DOIUrl":"10.1097/CM9.0000000000004371","url":null,"abstract":"<p><strong>Background: </strong>The immunosuppressive tumor microenvironment (TME) represents a major barrier to effective hepatocellular carcinoma (HCC) therapy. While interleukin-11 (IL-11) has been implicated in cancer progression, its immunomodulatory functions and underlying mechanisms in HCC remain poorly understood.</p><p><strong>Methods: </strong>We evaluated IL-11 expression and its clinical relevance using data from public databases and clinical HCC specimens. Functional effects of IL-11 were assessed through in vitro cell culture models and in vivo orthotopic tumor experiments in mice. Regulatory T (Treg) cell differentiation and TME composition were analyzed via flow cytometry and immunohistochemistry. Molecular mechanisms were explored using Western blotting, quantitative reverse transcription polymerase chain reaction (qRT-PCR), chromatin immunoprecipitation, and metabolic assays, focusing on the IL-11/methyl-CpG binding domain protein 3 (MBD3)/apolipoprotein H (APOH) pathway.</p><p><strong>Results: </strong>IL-11 was significantly overexpressed in HCC tissues and correlated with poor patient survival. Functionally, IL-11 enhanced the malignant phenotypes of HCC cells in vitro and in vivo , whereas its knockdown suppressed tumor migration and growth. Importantly, IL-11 increased the proportion of Treg cells in the HCC microenvironment by driving their differentiation, thereby fostering an immunosuppressive TME. Mechanistically, IL-11 upregulated MBD3, which transcriptionally repressed APOH. This downregulation activated the AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ (PPARγ)-mediated fatty acid oxidation (FAO) pathway, and pharmacological inhibition of FAO effectively reversed IL-11-induced Treg differentiation and tumor growth.</p><p><strong>Conclusion: </strong>We have identified a novel IL-11/MBD3/APOH/FAO regulatory axis that promotes HCC progression by enhancing Treg cell differentiation and establishing an immunosuppressive microenvironment. These results nominate IL-11 as a promising therapeutic target for HCC immunotherapy and shed new light on the metabolic basis of immune evasion in liver cancer.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sublethal heat stress-induced HSF4 upregulation via GRSF1 in an m6A-dependent manner in hepatocellular carcinoma.","authors":"Jie Chen, Yan Tan, Wei Xie, Lei Shi, Hu Quan, Hua Xiao, Jia Liu, Xianhai Mao, Pan Chen, Jia Luo","doi":"10.1097/CM9.0000000000004188","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004188","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Sublethal heat stress exacerbates hepatocellular carcinoma (HCC) by promoting recurrence and metastasis. This study aimed to investigate the molecular mechanisms by which sublethal heat stress enhances HCC progression to improve therapeutic strategies and patient outcomes in HCC management.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Cell-based and mouse models of insufficient thermal ablation in HCC were established via sublethal heat stress treatment. Twenty-four BALB/c nude mice were randomly divided into four groups, with six mice per group. RNA sequencing was used for transcriptional profiling. Messenger RNA (mRNA) and protein levels were quantified using quantitative reverse transcription polymerase chain reaction, Western blotting, and immunohistochemistry. Metastatic lesions in mouse liver and lung tissues were identified by hematoxylin and eosin staining. Proliferative, migratory, and invasive characteristics of tumor cells were probed via colony formation, 5-ethynyl-2'-deoxyuridine incorporation, scratch wound healing, and Transwell assays. Interactions between related genes were determined using dual-luciferase reporter, chromatin immunoprecipitation, co-immunoprecipitation, and RNA immunoprecipitation assays. Methylated RNA immunoprecipitation was used to detect N6-methyladenosine (m6A) levels in heat shock transcription factor 4 (HSF4).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;HSF4 was identified as a key gene that was upregulated in sublethal heat stress-treated cells (6.20-fold increase in Huh7 cells and 8.34-fold increase in Hep3B cells; P &lt;0.001). HSF4 knockdown inhibited sublethal heat stress-induced cell proliferation by 61.09% in Huh7 cells and 47.28% in Hep3B cells (P &lt;0.001 and P &lt;0.01), migration by 31.64% in Huh7 cells and 17.01% in Hep3B cells (P &lt;0.05), invasion by 29.68% in Huh7 cells and 47.03% in Hep3B cells (P &lt;0.05 and P &lt;0.001), and epithelial-mesenchymal transition (EMT). Furthermore, HSF4 knockdown repressed liver (reduced liver weight-to-body weight ratio by 32.46%, P &lt;0.001) and lung (decreased metastatic nodules from 10.5 to 5.17 per section, P &lt;0.001) metastases in vivo. Mechanistically, HSF4 increased cell cycle and apoptosis regulator 1 (CCAR1) levels and activated β-catenin pathway by binding to CCAR1 promoter. CCAR1 overexpression counteracted the suppressive effects of HSF4 knockdown on cell proliferation, migration, invasion, and EMT following sublethal heat stress. In addition, sublethal heat stress increased the HSF4 levels by upregulating guanine-rich RNA sequence binding factor 1 (GRSF1) (2.92-fold in Huh7 cells and 2.87-fold in Hep3B cells, P &lt;0.001) in an insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)-m6A-dependent manner. HSF4 overexpression blocked the inhibitory effects of GRSF1 knockdown on HCC cell proliferation and metastasis following sublethal heat stress.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Sublethal heat stress increased HSF4 expression by upregulating GRSF1 thro","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2F7 promotes lung adenocarcinoma progression by affecting phosphorylation and stabilization of β-catenin.","authors":"Sisi Chen, Manxiang Li, Jian Liu, Kai Li, Jiaojiao Zhang, Xinming Xie, Yamei Pang","doi":"10.1097/CM9.0000000000004312","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004312","url":null,"abstract":"<p><strong>Background: </strong>E2F transcription factor 7 (E2F7) has been implicated in the tumorigenesis and progression of multiple cancer types; however, the molecular mechanisms through which E2F7 regulates malignant phenotypes in cancer cells remain largely undefined. In this study, we investigated the biological functions and underlying mechanisms of E2F7 in lung adenocarcinoma (LUAD).</p><p><strong>Methods: </strong>E2F7 expression in LUAD was analyzed using The Cancer Genome Atlas (TCGA) datasets and further validated in clinical specimens via quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry. The effects of E2F7 on cancer cell self‑renewal and epithelial-mesenchymal transition (EMT) were assessed using sphere formation and Transwell assays, respectively. In vivo tumorigenicity and metastasis were evaluated using xenograft models combined with extreme limiting dilution analysis to assess tumor-initiating capacity. Wnt/β‑catenin pathway activity was measured using T-cell factor optimal promoter luciferase reporter plasmid/far-from optimal promoter luciferase reporter plasmid (TOP/FOP) flash reporter assays. β‑Catenin expression, stability, and ubiquitination were examined via western blotting, cycloheximide chase assays, and ubiquitination assays. Protein-protein interactions among E2F7, β‑catenin, and glycogen synthase kinase 3 beta (GSK3β) were verified through co‑immunoprecipitation (Co‑IP), glutathione S‑transferase (GST) pull‑down, and immunofluorescence assays. Truncated mutants were generated to map the functional binding domains of E2F7. In vitro immunoprecipitation and kinase assays were further performed to confirm that E2F7 regulates GSK3β autophosphorylation and β‑catenin phosphorylation.</p><p><strong>Results: </strong>Bioinformatic analyses revealed that E2F7 was significantly upregulated in LUAD tissues, and elevated E2F7 expression correlated with poor patient prognosis. Functional assays demonstrated that E2F7 promoted LUAD cell self‑renewal and EMT. Mechanistically, cytoplasmic E2F7 directly associated with β‑catenin through its DNA‑binding domain (DBD) and PHA03247 domain. E2F7 modulated β‑catenin phosphorylation at Ser675 and Ser33/37/T41, thereby inhibiting ubiquitin‑mediated degradation and enhancing β‑catenin protein stability. Furthermore, E2F7 interacted with GSK3β and suppressed its autophosphorylation at Tyr216, concomitant with reduced β-catenin phosphorylation at Ser33/37/T41 and its accumulation.</p><p><strong>Conclusion: </strong>Collectively, these findings indicate that E2F7 drives LUAD malignant progression through regulation of the GSK3β/β‑catenin signaling axis and stabilization of β‑catenin. This study unveils a novel oncogenic mechanism of E2F7 in LUAD and identifies E2F7 as a promising therapeutic target for clinical intervention in LUAD.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning for early post-ESWL risk stratification of pancreatitis in chronic pancreatitis.","authors":"Sihuai Xiong, Wenda Sheng, Wenbin Zou, Nan Ru, Hui Chen, Hao Wu, Jun Pan, Bo Li, Lei Xin, Xinying Tang, Lianghao Hu, Zhendong Jin, Yiqi Du, Luowei Wang, Zhaoshen Li, Yangyang Qian, Zhuan Liao","doi":"10.1097/CM9.0000000000004320","DOIUrl":"10.1097/CM9.0000000000004320","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting metabolic reprogramming in persister cancer cells: Emerging insights and therapeutic opportunities.","authors":"Siqi Li, Chunxiu Xiao, Jinxing Huang, Jinghong Xian, Kai Xiao","doi":"10.1097/CM9.0000000000004238","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004238","url":null,"abstract":"<p><strong>Abstract: </strong>Persister cancer cells (PCCs) constitute a transient tumor subpopulation that survives anticancer therapy by entering a drug-tolerant state, characterized by enhanced stress resilience and profound metabolic adaptation. Unlike genetically resistant clones, PCCs rely on reversible metabolic adaptations centrally coordinated by mitochondria. This coordination enables a context-dependent metabolic switch between glycolysis and oxidative phosphorylation, augmented fatty acid oxidation, rewired amino acid metabolism, and autophagy-mediated nutrient recycling. Collectively, these adaptations maintain energy and redox homeostasis, allowing PCCs to evade apoptosis and ferroptosis. Critically, these unique metabolic features represent therapeutically exploitable vulnerabilities that can be targeted before the emergence of stable genetic resistance. This review systematically delineates the metabolic plasticity of PCCs across malignancies, emphasizing the role of mitochondria as an integration hub. Furthermore, we discuss emerging strategies to exploit these vulnerabilities, providing a conceptual framework to prevent acquired resistance by targeting metabolic persistence.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-invasive tests for early-stage liver fibrosis: Current advances and challenges.","authors":"Caihong Wang, Wen Zhang, Hong Li, Wenyue Wu, Ziyan Pan, Ruoyu Gao, Haodong Ma, Qiushuang Ji, Zhi Chen, Wei Chen, Hong You","doi":"10.1097/CM9.0000000000004311","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004311","url":null,"abstract":"<p><strong>Abstract: </strong>Early-stage liver fibrosis (F1-F2) constitutes a clinically silent yet pivotal phase during which therapeutic intervention may halt or reverse disease progression. However, its timely identification remains challenging given the limited sensitivity of currently non-invasive tests (NITs), including routine serological panels and elastography-based techniques. This review provides a comprehensive and systematic evaluation of the evolving diagnostic landscape aimed at addressing this unmet need. Established approaches are critically appraised alongside emerging next-generation NITs, including ultrasensitive serum biomarkers, molecular imaging probes targeting fibrogenic activity, and artificial intelligence (AI)-driven analysis of conventional imaging modalities. In addition, this review examines innovative diagnostic strategies based on alternative biofluids, including urine, exhaled breath, and saliva, as well as gut microbiota-derived biomarkers and multiomics-integrated models, all of which offer distinct pathophysiological insights and potential advantages in large-scale screening. Despite their considerable promise for improving the precision of early-stage fibrosis detection, these approaches face substantial barriers to clinical implementation, including challenges related to validation, standardization, and integration into existing diagnostic pathways. Addressing these limitations will be essential for establishing a robust, multidimensional diagnostic framework capable of enabling early detection, guiding timely intervention, and advancing the paradigm of hepatology toward effective disease prevention.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe pulmonary hypertension due to chronic lung disease: Relevant hemodynamic criteria from a multicenter cohort study.","authors":"Rui Zhang, Yan Wu, Sugang Gong, Qian Jiang, Xuesong Chen, Yanzhe Yu, Qinhua Zhao, Hongling Qiu, Cijun Luo, Huiting Li, Wenhui Wu, Yuqin Chen, Jinming Liu, Weiping Xie, Chunli Liu, Lan Wang","doi":"10.1097/CM9.0000000000004293","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004293","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-cirrhotic metabolic dysfunction associated fatty liver disease-related hepatocellular carcinoma ( nc MAFLD-HCC): A growing concern.","authors":"Fatema Safri, Liang Qiao, Jacob George","doi":"10.1097/CM9.0000000000004275","DOIUrl":"10.1097/CM9.0000000000004275","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Burden of mental disorders: Evidence from the Global Burden of Disease Study 2023.","authors":"Jianhui Guo, Huan Wang, Yanhua Chen, Yaqing Tan, Xindou Chen, Junyu Lu, Zhiyong Zou, Jing Li","doi":"10.1097/CM9.0000000000004280","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004280","url":null,"abstract":"<p><strong>Background: </strong>Mental disorders contribute significantly to the global disease burden, with marked regional variations. This study provides the most up-to-date assessment of trends in the burden of mental disorders worldwide and in China and compares the burden of mental disorders between China and other regions.</p><p><strong>Methods: </strong>We conducted a descriptive secondary analysis of publicly available estimates from the updated Global Burden of Disease Study 2023 (GBD 2023) for the period 1990-2023, covering the 6 World Health Organization (WHO) regions and China. We summarized prevalence, disability-adjusted life years (DALYs), age-standardized prevalence rates (ASPRs), and age-standardized DALY rates (ASDRs) by year, region, age, and sex. Future trends were projected using a Bayesian age-period-cohort model with second-order random-walk priors, and uncertainty was described using 95% uncertainty or credible intervals.</p><p><strong>Results: </strong>In 2023, 1171.64 million people suffered from mental disorders globally, resulting in 171.27 million DALYs. China accounted for 16.32% of global cases and 15.39% of global DALYs, ranking second worldwide for both measures. In China, mental disorders were the fourth leading cause of DALYs. Among these, anxiety and depressive disorders were the most prevalent and the leading contributors to the burden. From 2010 to 2023, the ASDR increased by 16.18%, with the largest increase in anxiety disorders (38.37%), eating disorders (21.84%), and autism spectrum disorders (ASDs, 21.20%). Anxiety and depressive disorders were more prevalent in females, whereas attention-deficit/hyperactivity disorder (ADHD), ASDs, and conduct disorders were more prevalent in males. Although the burden was concentrated on older adults, notable increases were also observed among young people. By 2035, the numbers of mental disorder cases and associated DALYs in China are projected to reach 209.6 million and 28.7 million, respectively.</p><p><strong>Conclusions: </strong>China faces a growing burden of mental health issues, particularly anxiety disorders, eating disorders, and ASD. Immediate development and implementation of comprehensive strategies are crucial to address the escalating mental health crisis in China.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}