MedNexus
2026年 · 第139卷第08期
出版日期 2026-04-20电子版 ￥0.00元￥100.00元
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Editorial
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用于拷贝数变异检测的靶向下一代测序：临床肿瘤学的最新进展Zhao Du, Jie Hu, Guannan Chen, Jinqiao Tang, Yongchao Yao, Binwu Ying, Wenchuang Hu
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004001
摘要
癌症发展是一个复杂的、多步骤的过程，从根本上由最终由体细胞遗传改变引起的不同因素驱动。拷贝数变异(CNV)被定义为由基因组的结构重排引起的超过50个碱基对的大基因组区段的获得或丢失。[
Review Article
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急慢性肝衰竭：从定义到发病机制和治疗Yifan Xu, Jingting Liu, Dabao Shang, Robim M Rodrigues, Yu Chen, Xiaogang Xiang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004005
摘要
The concept of acute-on-chronic liver failure (ACLF) has been widely accepted around the world since it was proposed nearly 30 years ago, but there are still no universal criteria for the definition and diagnosis of ACLF worldwide. In recent years, the key clinical features for describing ACLF, such as the underlying chronic liver diseases, acute intrahepatic or extrahepatic insults, acute hepatic decompensation, extrahepatic organ failure, short-term high mortality, and the reversible course of the disease, have gradually narrowed the differences and reached a consensus. The pathogenesis of ACLF has not been fully elucidated, and most relevant studies focus on systemic inflammation and immune dysfunction. In this review, we discuss the evolution in the clinical definition of ACLF during the last few years and suggest clear criteria for ACLF diagnostics. In addition, we summarize the current understanding of ACLF pathogenesis and review the latest therapeutic targets against this condition. Lastly, we present a novel experimental mouse model that has been proven to be instrumental for the assessment of novel potential therapies for ACLF.
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趋化因子-趋化因子受体轴：实体瘤微环境重编程的新兴免疫治疗范式Yang Zhao, Xueqian Wang, Tong Lei, Hezhe Lu, Yong Zhao, Guiying Wang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004009
摘要
Chemokines play a critical role in regulating immune cell infiltration and their interactions with cancer cells in the tumor microenvironment (TME). Disrupted chemokine gradients influence immune cell recruitment and activation, as well as tumor cell proliferation, metastasis, and angiogenesis. By modulating these processes, chemokines shape the immune landscape of the tumor microenvironment, driving either immunosuppressive or immunostimulatory responses with corresponding pro- or antitumor effects. Dysregulated expression of chemokines and their receptors is strongly associated with tumor initiation, progression, and clinical outcomes. As a result, the chemokine receptor axis has gained prominence as a therapeutic target in cancer immunotherapy. This review explores chemokine expression profiles across various tumor types and their receptor-mediated interactions with immune cells. It also summarizes current strategies to therapeutically target chemokine signaling, both as standalone interventions and in combination with other treatment modalities.
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治疗诱导的肿瘤免疫微环境重塑：免疫治疗的机制见解和意义Dongping Chen, Ruiqi Wu, Zhengyu Liu, Yuan Wei, Dongming Kuang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004035
摘要
The tumor immune microenvironment (TIME) plays a pivotal role in tumor initiation, progression, and therapeutic response, and is closely associated with long-term treatment efficacy. Notably, therapeutic interventions are not only influenced by the immune microenvironment but also actively remodel its cellular and molecular architecture. In recent years, advanced technologies such as single-cell sequencing, spatial transcriptomics, and other multi-omics approaches have provided unprecedented insights into the dynamic interplay between therapeutic modalities and the TIME, as well as the secondary microenvironmental changes that critically influence immunotherapy outcomes. In this review, we summarize therapy-induced remodeling of the TIME, elucidate the mechanisms by which these changes modulate immunotherapy responsiveness, and discuss potential strategies for therapeutic optimization. A deeper understanding of therapy-driven alterations in the TIME, empowered by emerging high-resolution technologies, will not only facilitate the monitoring and prediction of treatment efficacy but also guide the development of more precise and individualized combination treatment strategies.
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扩大无细胞DNA在肺部疾病早期诊断和监测中的作用Liuqing Yang, Yu Gu, Jun Shao, Li Zhang, Chengdi Wang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003955
摘要
Circulating cell-free DNA (cfDNA) has firmly established itself as a cornerstone of liquid biopsy, advancing the noninvasive diagnosis and monitoring of pulmonary diseases. Its molecular characteristics, particularly methylation profiles, fragmentation patterns, and mutations, now enable a range of clinical applications—from early detection of lung cancer to rapid pathogen identification and severity assessment in pneumonia, and to precise risk stratification in chronic conditions such as chronic obstructive pulmonary disease and asthma. Beyond diagnostic applications, dynamic changes in cfDNA levels and profiles provide critical insights into disease monitoring across a spectrum of pulmonary disorders. While challenges in detection sensitivity, analytical standardization, and clinical validation remain, the ongoing integration of multi-omics data and artificial intelligence is refining the predictive power of cfDNA-based models. Future developments are expected to consolidate the role of cfDNA analysis as an indispensable tool in precision pulmonology, ultimately transforming diagnostic pathways and enabling more personalized, proactive management of respiratory health.
Original Article
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1990年至2021年全球缺血性心脏病负担：2021年全球疾病负担研究的结果和2030年的预测Shengyu Jing, Ao Chen, Yan Xia, Jiaqi Ma, Danbo Lu, Zhangwei Chen, Juying Qian, Junbo Ge
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004006
摘要
Background:
Ischemic heart disease (IHD) remains the leading cause of global morbidity and mortality, yet comprehensive analyses of its burden across sociodemographic contexts and future projections are limited. This study leverages the Global Burden of Disease (GBD) 2021 database to assess the global, regional, and national burden of IHD from 1990 to 2021 and predicts trends up to 2030.
Methods:
Data on IHD prevalence, incidence, disability-adjusted life years (DALYs), and mortality were extracted from the GBD 2021 database. Age-standardized rates (ASRs) and estimated annual percentage changes (EAPCs) were calculated to evaluate temporal trends. The Bayesian Age-Period-Cohort (BAPC) model was employed to project age-standardized incidence rates (ASIRs) through 2030. Analyses were stratified by sociodemographic index (SDI), age, sex, and region.
Results:
From 1990 to 2021, global IHD cases increased by 127%, reaching 254.28 million, with the sharpest rises in East Asia and Andean Latin America. Age-standardized incidence, DALYs, and mortality rates declined globally (EAPC: -44%, -120%, and -130%). High-SDI regions exhibited significant reductions in mortality (EAPC: -130%), while low-, low-middle-, and middle-SDI regions faced rising burdens in some indications. Men had consistently higher rates than women, particularly in the elderly population. Projections suggest continued declines in ASIRs through 2030, driven largely by reductions among adults aged ≥70 years, while incidence among younger adults (30-49 years) is expected to fluctuate.
Conclusions:
Although the global absolute burden of IHD increased from 1990 to 2021, age-standardized rates declined, and the burden is projected to decrease further through 2030. These findings highlight the critical need for enhanced prevention and healthcare policies to address the global IHD burden effectively. In low- and middle-SDI regions, policy efforts should be intensified to control risk factors, whereas in high-SDI regions the focus should be on secondary prevention and rehabilitation.
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1990-2023年中国急性病毒性肝炎的国家趋势：2023年全球疾病负担更新分析Jingran Jiao, Xiao Che, Huixin Tang, Wenling Wang, Rui Zhao, Qingkun Song, Manman Xu, Yu Chen
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004010
摘要
Background:
The prerequisite for achieving the goal of the World Health Organization to completely eliminate viral hepatitis by 2030 is China’s accurate understanding of the current disease burden, thereby providing a basis for formulating and optimizing intervention measures.
Methods:
Based on the Global Burden of Disease (GBD) 2023 dataset, we extracted data on acute hepatitis A, B, C, and E in China, including incidence, mortality, disability-adjusted life years (DALYs), and their corresponding age-standardized rates (ASRs). To account for differences in age and sex distributions, we calculated ASRs based on the age-specific data extracted from the GBD 2023 dataset. To further assess temporal patterns across different age groups, we estimated the average annual percent change (AAPC). We applied the autoregressive integrated moving average model to project acute viral hepatitis (AVH) disease burden for 2024-2030.
Results:
In 2023, there were an estimated 48.7 million incidence cases of AVH in China, including approximately 19.0 million cases of acute hepatitis A (AHA), 19.2 million cases of acute hepatitis B (AHB), 1.35 million cases of acute hepatitis C (AHC), and 9.2 million cases of acute hepatitis E (AHE). From 1990 to 2023, the overall age-standardized incidence rates (ASIR) of the four major AVH types in China declined (AAPC = -0.90%, 95% confidence interval [CI]: -0.93% to -0.87%). In the previous decade, divergent trends were observed. The ASIR of AHC increased (AAPC = 1.42%, 95% CI: 1.39-1.46%), AHE remained stable (AAPC = -0.04%, 95% CI: -0.39-0.32%), whereas AHA and AHB decreased. Moreover, the age-standardized mortality and DALYs rates for AVH significantly decreased. Age-specific analysis further revealed an upward trend in standardized incidence among individuals aged 25-29 years (AAPC = 0.14%, 95% CI: 0.10-0.19%). A continued decline in the ASIR of AVH is projected for 2024-2030.
Conclusions:
In China, the overall burden of AVH has decreased between 1990 and 2023. AHB vaccination among younger populations should be strengthened, and targeted prevention and control strategies should be implemented for those at high risk of AHC, to curb the spread of the disease and reduce the overall burden.
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HER2状态分层的三阴性乳腺癌分子特征及预后Xia Yang, Jin Wang, Huimin An, Yongtao He, Yi Gan, Qi Chen, Bo Liu, Wangyang Tang, Guoxiang Fu, Zhinong Jiang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003942
摘要
Background:
Human epidermal growth factor receptor 2 (HER2)-low breast cancer (BC) is an emerging subtype with specific clinicopathological features and therapeutic strategies. However, limited studies are available on the molecular characteristics and prognosis of triple-negative breast cancer (TNBC).
Methods:
This study was conducted using the clinicopathological and genomic data of 1006 TNBC patients, which were extracted from The Cancer Genome Atlas (TCGA), Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), and Sir Run Run Shaw Hospital of Zhejiang University (SRRSH) cohorts. The clinicopathological features, survival outcomes, molecular characteristics, and immune profiles of TNBCs based on HER2 status were evaluated.
Results:
Patients were stratified into HER2-low (N = 676) and HER2-zero (N = 330) groups according to their HER2 status. We found HER2-low TNBCs had a lower histological grade and Ki67 index compared to the HER2-zero subgroup in the SRRSH cohort. However, no significant association has been found between the HER2 status and the disease-free survival (DFS), recurrence-free survival (RFS), or overall survival (OS) in TNBCs. Genomic mutation analysis showed that the HER2-low TNBCs exhibited higher mutated frequencies of PIK3CA, MUC17, and PTEN, while FAT3, RYR2, and CSMD3 were more frequently mutated in the HER2-zero subgroup. Furthermore, the combined mutation of PIK3CA and MUC17, which had a higher frequency in the HER2-low subgroup, was associated with poorer survival in TNBCs. Immune profile analysis revealed a higher percentage of plasma cells in patients with low HER2 expression.
Conclusion:
Taken together, our study reflected the impact of the HER2 status on the clinicopathological and molecular features of TNBCs, which might offer additional introspection and improvement for translational studies and therapeutic decisions for TNBCs.
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S6K1过表达通过诱导乳腺癌细胞的翻译增强自噬CLUXingmei Shu, Ranjiaxi Wang, Yan Liu, Xiaoqian Shi, Yuhao Liu, Yinan Chen, Jinming Shi, Mingyang Liu, Yongmei Song, Dan Li
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003596
摘要
Background:
Ribosomal protein S6 kinase B1 (S6K1) is frequently amplified and correlates with drug resistance and poor prognosis in patients with breast cancer. Although S6K1 functions primarily in the process of translation, the genome-wide translational profiles regulated by S6K1 remain unclear. This study sought to clarify the pivotal role of S6K1 in translational regulation and investigate its novel targets in breast cancer.
Methods:
Ribosome profiling sequencing (Ribo-seq) was performed to explore genome-wide translational profiles regulated by S6K1 in breast cancer cells. Integrated multiomics analyses, including Ribo-seq, RNA sequencing, and mass spectrometry, were employed to identify a new target of S6K1 translational regulation, the autophagy-related gene clusterin (CLU). Western blotting and immunofluorescence were utilized to confirm that S6K1 regulated CLU translation, thus influencing autophagy in breast cancer cells. Bafilomycin A1 (a late-stage autophagy inhibitor) was used to demonstrate that S6K1 regulated autophagosome formation in breast cancer cells through affecting the translation of CLU.
Results:
S6K1 depletion resulted in the downregulation of global messenger RNA (mRNA) translation and affected translation in multiple pathways that play crucial roles in carcinogenesis, with autophagy-related pathways being the most prominently affected. The role of S6K1 in autophagy was further confirmed in breast cancer cells, and CLU was identified as a novel target regulated by S6K1 at the translational level. Additionally, the overexpression of S6K1 promoted the translation of CLU, thus facilitating the formation of autophagosomes.
Conclusion:
This study demonstrated that the overexpression of S6K1 promoted autophagy in breast cancer cells by facilitating the translation of the autophagy-related gene CLU.
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克隆性造血与未来疾病和死亡率相关Weishi Liu, Yueting Deng, Liu Yang, Ziyi Wang, Lingzhi Ma, Yuming Xu, Qiang Dong, Jianfeng Feng, Wei Cheng, Jintai Yu
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003782
摘要
Background:
Clonal hematopoiesis is a proposed marker of aging. Clonal hematopoiesis of indeterminate potential (CHIP) is a candidate risk factor for atherosclerotic cardiovascular diseases, hematological malignancies, and all-cause mortality, while its associations with the diseases of other systems and cause-specific mortality remain inconclusive.
Methods:
We estimated the longitudinal risk for CHIP with 70 common diseases, all-cause, and cause-specific mortality among 431,546 participants in the UK Biobank. Two-sample Mendelian randomization analyses were performed to test the causal associations of CHIP with incident diseases. Cox proportional hazard regression model was used to generate the hazard ratio [HR] and 95% confidence interval [CI] for each CHIP phenotype with the common health-related outcomes. Also evaluated the joint associations between CHIP and telomere length for diseases and mortalities.
Results:
This study included 431,546 participants (mean age, 56.49 years; 45.7% male), of whom 20,274 had CHIP. CHIP at baseline was associated with increased risk of cancers (HR = 1.14, 95% CI 1.10-1.17), infections (HR = 1.12, 95% CI 1.07-1.16), ischemic heart diseases (HR = 1.07, 95% CI 1.02-1.12), diseases of the blood (HR = 1.31, 95% CI 1.26-1.37), nervous (HR = 1.05, 95% CI 1.01-1.10), respiratory (HR = 1.10, 95% CI 1.06-1.13), and genitourinary systems (HR = 1.10, 95% CI 1.07-1.14), and related mortality (false discovery rate <0.05). CHIP carriers were also at elevated risk of incident mental (HR = 1.07, 95% CI 1.03-1.12) and dermatological (HR = 1.07, 95% CI 1.03-1.11) disorders and mortality due to circulatory system (HR = 1.19, 95% CI 1.11-1.28). Most of the associations between CHIP and diseases or mortalities were robust after adjustment for inflammatory parameters. Large clone size CHIP had higher longitudinal risks compared with small clone size or overall CHIP. CHIP due to TET2 mutation was associated with more outcomes than other common CHIP driver genes. Significant interactions were observed between CHIP and short telomere length, the additive and multiplicative effects on the risk of diseases and mortalities were more obvious among large clone size CHIP.
Conclusion:
This study showed that CHIP was associated with diseases and mortalities of multiple systems, suggesting CHIP was a candidate risk factor for human health.
Correspondence
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缺氧相关视网膜/脉络膜血管疾病的发病机制及机制Rong Xue, Shenzhi Liang, Guangming Wan
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003569
摘要
致编辑：视网膜是人体最耗氧的组织之一，对缺氧特别敏感。缺氧可导致血管生长因子、细胞因子、趋化因子和其他细胞介质的表达失衡，可能导致血管血液渗漏和新生血管形成，最终导致失明或严重的视力损害。缺氧是与各种视网膜/脉络膜血管疾病相关的病理风险因素，例如糖尿病视网膜病变(DR)、视网膜静脉阻塞(RVO)、早产儿视网膜病变(ROP)和湿性年龄相关性黄斑变性(AMD)，其影响所有年龄的人，包括儿童、工作成人和老年人。
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1990-2021年中国孕产妇疾病负担趋势及次国家差异Yuchen Zou, Yeerlin Asihaer, Menglong Li, Huiming He, Nourhan M. Khattab, Galal Elshishiney, Jinlei Qi, Peng Yin, Lijun Wang, Maigeng Zhou 等
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004013
摘要
致编辑：从1990年到2021年，中国孕产妇疾病负担发生了显著变化。中国在解决影响孕妇福祉的复杂因素方面面临挑战。社会经济差异、医疗基础设施的地区差异以及医疗质量的差距仍然是弱势群体实现最佳健康结果的重大障碍。[
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儿童川崎病冠状动脉旁路移植术的中期结果：中国多中心回顾性研究Xiaomin He, Kai Ma, Jiawei Shi, Yonggang Li, Yusheng Pang, Lin Han, Jie Shen, Jinghao Zheng, Shoujun Li, Hao Zhang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004045
摘要
致编辑：川崎病（KD）是儿童期最常见的全身性血管炎。KD的冠状动脉并发症已成为儿童获得性心脏病的重要原因。[
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临床特征和APOE中国脂蛋白肾小球病患者的变异谱Mengshi Li, Yang Li, Lei Jiang, Xin Wang, Zhiying Liu, Zhuoran Song, Ruilian You, Yuqing Chen, Xujie Zhou, Hong Zhang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003978
摘要
致编辑：脂蛋白肾小球病（LPG）是一种罕见的肾脏疾病，其特征是肾小球毛细血管中的脂蛋白血栓。临床上表现为蛋白尿，常进展为进行性肾功能不全。[
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小于胎龄儿与精神障碍的关系Anran Tian, Furong Liang, Fucheng Meng, Sujuan Li, Cai Zhang, Xiaoping Luo
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004002
摘要
致编辑：小于胎龄儿（SGA）通常定义为出生体重低于平均值至少2个标准差或低于胎龄儿的第10百分位。SGA儿童面临更高的晚年疾病风险，特别是神经系统并发症，并且比出生时适合胎龄（AGA）的儿童有更高的认知、社会情感和行为困难率。SGA的长期认知影响，如较低的智商（IQ）和学业不良，已被很好地记录，但与SGA相关的精神障碍尚未得到系统的描述。注意缺陷多动障碍（ADHD）和自闭症谱系障碍（ASD）是普遍的神经发育疾病，对生活质量有重大的长期影响。[
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多系统萎缩患者轻度认知障碍的亚型及预测因素Yu Guo, Yunchuang Sun, Ruying Yuan, Lihua Dong, Meng Zhao, Zhiyu Lv, Wei Zhang, Yaru Zhang, Yuyuan Huang, Shufen Chen 等
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003866
摘要
致编辑：多系统萎缩（MSA）是一种罕见的神经退行性疾病，进展缓慢，预后不良。[
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人羊膜上皮干细胞通过Notch信号通路促进胆管损伤胆管细胞再生Zhoucheng Wang, Wenwen Ge, Xiao Tang, Jun Chen, Jinying Li, Luyang Yu, Kai Wang, Xiao Xu
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003557
摘要
致编辑：胆管损伤（BDI）极大地影响肝移植（LT）后的预后。[
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急性泛发性发疹性脓疱病与泛发性脓疱型银屑病的临床鉴别：一项多中心研究Shuxian Guo, Xuming Wang, Wenhao Cheng, Zuoyao Qi, Yao Sun, Linlin Ma, Fanxiang Wang, Guan Jiang
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000003812
摘要
致编辑：急性泛发性发疹性脓疱病（AGEP）和泛发性脓疱型银屑病（GPP）均表现为广泛的无菌脓疱，有时形成大脓疱湖，并具有重叠的临床和组织学特征。[
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甲状腺癌与维生素D缺乏的关系Tianyi Lv, Jing Feng, Lili Cui, Junyu Zhao, Lin Liao
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004030
摘要
致编辑：甲状腺癌（TC）是全球发病率增长最快的癌症之一。研究发现，性别、遗传、硒和不利的生活方式都与TC的风险有关。然而，维生素D（VD）缺乏是否与TC有关仍不清楚。
Comment
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打破时间障碍幽门螺杆菌再治疗：多维视角的见解Jingyuan Xu, Renchun Du, Nonghua Lu, Yin Zhu, Yi Hu
中华医学杂志英文版2026年 139卷 08期
DOI: 10.1097/CM9.0000000000004023
摘要
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