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中国科学:生命科学（英文版）
中国科学:生命科学（英文版）

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中国科学:生命科学（英文版）/Journal Science China(Life Sciences)CSCDCSTPCDSCI
查看更多>>《中国科学》是中国科学院主办、中国科学杂志社出版的自然科学专业性学术刊物。《中国科学》任务是反映中国自然科学各学科中的最新科研成果，以促进国内外的学术交流。《中国科学》以论文形式报道中国基础研究和应用研究方面具有创造性的、高水平的和有重要意义的科研成果。在国际学术界，《中国科学》作为代表中国最高水平的学术刊物也受到高度重视。国际上最具有权威的检索刊物SCI，多年来一直收录《中国科学》的论文。1999年《中国科学》夺得国家期刊奖的第一名。
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    Progress in gut microbiota-host interaction

    Changtao Jiang
    851-853页
      原文链接:
    • 万方数据
    • 维普

    When smoke meets gut:deciphering the interactions between tobacco smoking and gut microbiota in disease development

    Bo ChenGuangyi ZengLulu SunChangtao Jiang...
    854-864页
    查看更多>>摘要：Tobacco smoking is a prevalent and detrimental habit practiced worldwide,increasing the risk of various diseases,including chronic obstructive pulmonary disease(COPD),cardiovascular disease,liver disease,and cancer.Although previous research has explored the detrimental health effects of tobacco smoking,recent studies suggest that gut microbiota dysbiosis may play a critical role in these outcomes.Numerous tobacco smoke components,such as nicotine,are found in the gastrointestinal tract and interact with gut microbiota,leading to lasting impacts on host health and diseases.This review delves into the ways tobacco smoking and its various constituents influence gut microbiota composition and functionality.We also summarize recent advancements in understanding how tobacco smoking-induced gut microbiota dysbiosis affects host health.Furthermore,this review introduces a novel perspective on how changes in gut microbiota following smoking cessation may contribute to withdrawal syndrome and the degree of health improvements in smokers.
      原文链接:
    • 万方数据
    • 维普

    Bile acid signaling in the regulation of whole body metabolic and immunological homeostasis

    Wei JiaYitao LiKenneth C.P.CheungXiaojiao Zheng...
    865-878页
    查看更多>>摘要：Bile acids(BAs)play a crucial role in nutrient absorption and act as key regulators of lipid and glucose metabolism and immune home-ostasis.Through the enterohepatic circulation,BAs are synthesized,metabolized,and reabsorbed,with a portion entering the vascular circulation and distributing systemically.This allows BAs to interact with receptors in all major organs,leading to organ-organ interactions that regulate both local and global metabolic processes,as well as the immune system.This review focuses on the whole-body effects of BA-mediated metabolic and immunological regulation,including in the brain,heart,liver,intestine,eyes,skin,adipose tissue,and muscle.Targeting BA synthesis and receptor signaling is a promising strategy for the development of novel therapies for various diseases throughout the body.
      原文链接:
    • 万方数据
    • 维普

    High-fat diet impairs gut barrier through intestinal microbiota-derived reactive oxygen species

    Nianyi ZengFan WuJunqi LuXiang Li...
    879-891页
    查看更多>>摘要：Gut barrier disruption is a key event in bridging gut microbiota dysbiosis and high-fat diet(HFD)-associated metabolic disorders.However,the underlying mechanism remains elusive.In the present study,by comparing HFD-and normal diet(ND)-treated mice,we found that the HFD instantly altered the composition of the gut microbiota and subsequently damaged the integrity of the gut barrier.Metagenomic sequencing revealed that the HFD upregulates gut microbial functions related to redox reactions,as confirmed by the increased reactive oxygen species(ROS)levels in fecal microbiota incubation in vitro and in the lumen,which were detected using in vivo fluorescence imaging.This microbial ROS-producing capability induced by HFD can be transferred through fecal microbiota transplantation(FMT)into germ-free(GF)mice,downregulating the gut barrier tight junctions.Similarly,mono-colonizing GF mice with an Enterococcus strain excelled in ROS production,damaged the gut barrier,induced mitochondrial malfunction and apoptosis of the intestinal epithelial cells,and exacerbated fatty liver,compared with other low-ROS-producing Enterococcus strains.Oral administration of recombinant high-stability-superoxide dismutase(SOD)significantly reduced intestinal ROS,protected the gut barrier,and improved fatty liver against the HFD.In conclusion,our study suggests that extracellular ROS derived from gut microbiota play a pivotal role in HFD-induced gut barrier disruption and is a potential therapeutic target for HFD-associated metabolic diseases.
      原文链接:
    • 万方数据
    • 维普

    Exercise-induced microbial changes in preventing type 2 diabetes

    Ting YaoHui WangKaiqing LinRuwen Wang...
    892-899页
    查看更多>>摘要：The metabolic benefits associated with long-term physical activity are well appreciated and growing evidence suggests that it involves the gut microbiota.Here we re-evaluated the link between exercise-induced microbial changes and those associated with prediabetes and diabetes.We found that the relative abundances of substantial amounts of diabetes-associated metagenomic species associated negatively with physical fitness in a Chinese athlete students cohort.We additionally showed that those microbial changes correlated more with handgrip strength,a simple but valuable biomarker suggestive of the diabetes states,than maximum oxygen intake,one of the key surrogates for endurance training.Moreover,the causal relationships among exercise,risks for diabetes,and gut microbiota were explored based on mediation analysis.We propose that the protective roles of exercise against type 2 diabetes are mediated,at least partly,by the gut microbiota.
      原文链接:
    • 万方数据
    • 维普

    Pseudomonas aeruginosa regulator PvrA binds simultaneously to multiple pseudo-palindromic sites for efficient transcription activation

    Yibo ZhuBingnan LuoXingyu MouYingjie Song...
    900-912页
    查看更多>>摘要：Tetracycline repressor(TetR)family regulators(TFRs)are the largest group of DNA-binding transcription factors and are widely distributed in bacteria and archaea.TFRs play vital roles in controlling the expression of various genes and regulating diverse physiological processes.Recently,a TFR protein Pseudomonas virulence regulator A(PvrA),was identified from Pseudomonas aeruginosa as the transcriptional activator of genes involved in fatty acid utilization and bacterial virulence.Here,we show that PvrA can simultaneously bind to multiple pseudo-palindromic sites and upregulate the expression levels of target genes.Cryo-electron microscopy(cryo-EM)analysis indicates the simultaneous DNA recognition mechanism of PvrA and suggests that the bound DNA fragments consist of a distorted B-DNA double helix.The crystal structure and functional analysis of PvrA reveal a hinge region that secures the correct domain motion for recognition of the promiscuous promoter.Additionally,our results showed that mutations disrupting the regulatory hinge region have differential effects on biofilm formation and pyocyanin biosynthesis,resulting in attenuated bacterial virulence.Collectively,these findings will improve the understanding of the relationship between the structure and function of the TetR family and provide new insights into the mechanism of regulation of P.aeruginosa virulence.
      原文链接:
    • 万方数据
    • 维普

    Chinese Society of Cardiology guidelines on the diagnosis and treatment of adult fulminant myocarditis

    Chinese Society of Cardiology,Chinese Medical Association,Writing GroupJiangang JiangHongyang ShuDao Wen Wang...
    913-939页
    查看更多>>摘要：Fulminant myocarditis is an acute diffuse inflammatory disease of myocardium.It is characterized by acute onset,rapid progress and high risk of death.Its pathogenesis involves excessive immune activation of the innate immune system and formation of inflammatory storm.According to China's practical experience,the adoption of the"life support-based comprehensive treatment regimen"(with mechanical circulation support and immunomodulation therapy as the core)can significantly improve the survival rate and long-term prognosis.Special emphasis is placed on very early identification,very early diagnosis,very early prediction and very early treatment.
      原文链接:
    • 万方数据
    • 维普

    Role of adhesion molecules in cancer and targeted therapy

    Chunmei FanFang XiongShanshan ZhangZhaojian Gong...
    940-957页
    查看更多>>摘要：Adhesion molecules mediate cell-to-cell and cell-to-extracellular matrix interactions and transmit mechanical and chemical signals among them.Various mechanisms deregulate adhesion molecules in cancer,enabling tumor cells to proliferate without restraint,invade through tissue boundaries,escape from immune surveillance,and survive in the tumor microenvironment.Recent studies have revealed that adhesion molecules also drive angiogenesis,reshape metabolism,and are involved in stem cell self-renewal.In this review,we summarize the functions and mechanisms of adhesion molecules in cancer and the tumor microenvironment,as well as the therapeutic strategies targeting adhesion molecules.These studies have implications for furthering our understanding of adhesion molecules in cancer and providing a paradigm for exploring novel therapeutic approaches.
      原文链接:
    • 万方数据
    • 维普

    Pivotal role for long noncoding RNAs in zygotic genome activation in mice

    Kang ChenWenju LiuJiang ZhuXiaochen Kou...
    958-969页
    查看更多>>摘要：Vertebrate life begins with fertilization,and then the zygote genome is activated after transient silencing,a process termed zygotic genome activation(ZGA).Despite its fundamental role in totipotency and the initiation of life,the precise mechanism underlying ZGA initiation remains unclear.The existence of minor ZGA implies the possible critical role of noncoding RNAs in the initiation of ZGA.Here,we delineate the expression profile of long noncoding RNAs(lncRNAs)in early mouse embryonic development and elucidate their critical role in minor ZGA.Compared with protein-coding genes(PCGs),lncRNAs exhibit a stronger correlation with minor ZGA.Distinct H3K9me3 profiles can be observed between lncRNA genes and PCGs,and the enrichment of H3K9me3 before ZGA might explain the suspended expression of major ZGA-related PCGs despite possessing PolⅡ pre-configuration.Furthermore,we identified the presence of PolⅡ-enriched MuERV-L around the transcriptional start site of minor ZGA-related lncRNAs,and these repeats are responsible for the activation of minor ZGA-related lncRNAs and subsequent embryo development.Our study suggests that MuERV-L mediates minor ZGA lncRNA activation as a critical driver between epigenetic reprogramming triggered by fertilization and the embryo developmental program,thus providing clues for under-standing the regulatory mechanism of totipotency and establishing bona fide totipotent stem cells.
      原文链接:
    • 万方数据
    • 维普

    Exosome-encapsulated IncRNA HOTAIRM1 contributes to PM2.5-aggravated COPD airway remodeling by enhancing myofibroblast differentiation

    Huaqi GuoLuo FeiHengyi YuYan Li...
    970-985页
    查看更多>>摘要：Emphysema,myofibroblast accumulation and airway remodeling can occur in the lungs due to exposure to atmospheric pollution,especially fine particulate matter(PM2.5),leading to chronic obstructive pulmonary disease(COPD).Specifically,bronchial epithelium-fibroblast communication participates in airway remodeling,which results in COPD.An increasing number of studies are now being conducted on the role of exosome-mediated cell-cell communication in disease pathogenesis.Here,we investigated whether exosomes generated from bronchial epithelial cells could deliver information to normal stromal fibroblasts and provoke cellular responses,resulting in airway obstruction in COPD.We studied the mechanism of exosome-mediated intercellular communication between human bronchial epithelial(HBE)cells and primary lung fibroblasts(pLFs).We found that PM2.5-induced HBE-derived exosomes promoted myofibroblast differentiation in pLFs.Then,the exosomal lncRNA expression profiles derived from PM2.5-treated HBE cells and nontreated HBE cells were investigated using an Agilent Human LncRNA Array.Combining coculture assays and direct exosome treatment,we found that HBE cell-derived exosomal HOTAIRM1 facilitated the myofibroblast differentiation of pLFs.Surprisingly,we discovered that exosomal HOTAIRM1 enhanced pLF proliferation to secrete excessive collagen secretion,leading to airway obstruction by stimulating the TGF-β/SMAD3 signaling pathway.Significantly,PM2.5 reduced FEV1/FVC and FEV1 and increased the level of serum exosomal HOTAIRM1 in healthy people;moreover,serum exosomal HOTAIRM1 was associated with PM2.5-related reductions in FEV1/FVC and FVC.These findings show that PM2.5 triggers al-terations in exosome components and clarify that one of the paracrine mediators of myofibroblast differentiation is bronchial epithelial cell-derived HOTAIRM1,which has the potential to be an effective prevention and therapeutic target for PM2.5-induced COPD.
      原文链接:
    • 万方数据