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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）

周光召

月刊

1674-7305

sales@scichina.org

010-64019820

100717

北京东黄城根北街16号

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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    BioTreasury:a community-based repository enabling indexing and rating of bioinformatics tools

    Qi ZhaoXin ZhouJingxing WuJieyi Cai...
    221-229页
    查看更多>>摘要：The exponential growth of bioinformatics tools in recent years has posed challenges for scientists in selecting the most suitable one for their data analysis assignments.Therefore,to aid scientists in making informed choices,a community-based platform that indexes and rates bioinformatics tools is urgently needed.In this study,we introduce BioTreasury(http://biotreasury.rjmart.cn),an integrated community-based repository that provides an interactive platform for users and developers to share their experiences in various bioinformatics tools.BioTreasury offers a comprehensive collection of well-indexed bioinformatics software,tools,and databases,totaling over 10,000 entries.In the past two years,we have continuously improved and maintained BioTreasury,adding several exciting features,including creating structured homepages for every tool and user,a hierarchical category of bioinformatics tools and classifying tools using large language model(LLM).BioTreasury streamlines the tool submission process with intelligent auto-completion.Additionally,BioTreasury provides a wide range of social features,for example,enabling users to participate in interactive discussions,rate tools,build and share tool collections for the public.We believe BioTreasury can be a valuable resource and knowledge-sharing platform for the biomedical community.It empowers researchers to effectively discover and evaluate bioinformatics tools,fostering collaboration and advancing bioinformatics re-search.
      原文链接:
    • 万方数据
    • 维普

    Stay in touch with the endoplasmic reticulum

    Sha SunGan ZhaoMingkang JiaQing Jiang...
    230-257页
    查看更多>>摘要：The endoplasmic reticulum(ER),which is composed of a continuous network of tubules and sheets,forms the most widely distributed membrane system in eukaryotic cells.As a result,it engages a variety of organelles by establishing membrane contact sites(MCSs).These contacts regulate organelle positioning and remodeling,including fusion and fission,facilitate precise lipid exchange,and couple vital signaling events.Here,we systematically review recent advances and converging themes on ER-involved organellar contact.The molecular basis,cellular influence,and potential physiological functions for ER/nuclear envelope contacts with mitochondria,Golgi,endosomes,lysosomes,lipid droplets,autophagosomes,and plasma membrane are summarized.
      原文链接:
    • 万方数据
    • 维普

    Whole-genome sequencing in medicinal plants:current progress and prospect

    Yifei PeiLiang LengWei SunBaocai Liu...
    258-273页
    查看更多>>摘要：Advancements in genomics have dramatically accelerated the research on medicinal plants,and the development of herbgenomics has promoted the"Project of 1K Medicinal Plant Genome"to decipher their genetic code.However,it is difficult to obtain their high-quality whole genomes because of the prevalence of polyploidy and/or high genomic heterozygosity.Whole genomes of 123 medicinal plants were published until September 2022.These published genome sequences were investigated in this review,covering their classification,research teams,ploidy,medicinal functions,and sequencing strategies.More than 1,000 institutes or universities around the world and 50 countries are conducting research on medicinal plant genomes.Diploid species account for a majority of sequenced medicinal plants.The whole genomes of plants in the Poaceae family are the most studied.Almost 40％of the published papers studied species with tonifying,re-plenishing,and heat-cleaning medicinal effects.Medicinal plants are still in the process of domestication as compared with crops,thereby resulting in unclear genetic backgrounds and the lack of pure lines,thus making their genomes more difficult to complete.In addition,there is still no clear routine framework for a medicinal plant to obtain a high-quality whole genome.Herein,a clear and complete strategy has been originally proposed for creating a high-quality whole genome of medicinal plants.Moreover,whole genome-based biological studies of medicinal plants,including breeding and biosynthesis,were reviewed.We also advocate that a research platform of model medicinal plants should be established to promote the genomics research of medicinal plants.
      原文链接:
    • 万方数据
    • 维普

    Challenges and opportunities in rare cancer research in China

    Jianxin XueQunyan Lyu
    274-285页
    查看更多>>摘要：Cancer is one of the major public health challenges in China.Rare cancers collectively account for a considerable proportion of all malignancies.The lack of awareness of rare cancers among healthcare professionals and the general public,the typically complex and delayed diagnosis,and limited access to clinical trials are key challenges.Recent years have witnessed an increase in funding for research related to rare cancers in China.In this review,we provide a comprehensive overview of rare cancers and summarize the status of research on rare cancers in China and overseas,including the trends of funding and publications.We also highlight the challenges and perspectives regarding rare cancers in China.
      原文链接:
    • 万方数据
    • 维普

    High-density lipoprotein regulates angiogenesis by affecting autophagy via miRNA-181a-5p

    Bi-Ang KangHua-Ming LiYa-Ting ChenMeng-Jie Deng...
    286-300页
    查看更多>>摘要：We previously demonstrated that normal high-density lipoprotein(nHDL)can promote angiogenesis,whereas HDL from patients with coronary artery disease(dHDL)is dysfunctional and impairs angiogenesis.Autophagy plays a critical role in angiogenesis,and HDL regulates autophagy.However,it is unclear whether nHDL and dHDL regulate angiogenesis by affecting autophagy.Endothelial cells(ECs)were treated with nHDL and dHDL with or without an autophagy inhibitor.Autophagy,endothelial nitric oxide synthase(eNOS)expression,miRNA expression,nitric oxide(NO)production,superoxide anion(O2·-)generation,EC migration,and tube formation were evaluated.nHDL suppressed the expression of miR-181a-5p,which promotes autophagy and the expression of eNOS,resulting in NO production and the inhibition of O2·-generation,and ultimately increasing in EC migration and tube formation.dHDL showed opposite effects compared to nHDL and ultimately inhibited EC migration and tube formation.We found that autophagy-related protein 5(ATG5)was a direct target of miR-181a-5p.ATG5 silencing or miR-181a-5p mimic inhibited nHDL-induced autophagy,eNOS expression,NO production,EC migration,tube formation,and enhanced O2·-generation,whereas overexpression of ATG5 or miR-181a-5p inhibitor reversed the above effects of dHDL.ATG5 expression and angiogenesis were decreased in the ischemic lower limbs of hypercholesterolemic low-density lipoprotein receptor null(LDLr-/-)mice when compared to C57BL/6 mice.ATG5 overexpression improved angiogenesis in ischemic hypercholester-olemic LDLr-/-mice.Taken together,nHDL was able to stimulate autophagy by suppressing miR-181a-5p,subsequently increasing eNOS expression,which generated NO and promoted angiogenesis.In contrast,dHDL inhibited angiogenesis,at least partially,by increasing miR-181a-5p expression,which decreased autophagy and eNOS expression,resulting in a decrease in NO production and an increase in O2·-generation.Our findings reveal a novel mechanism by which HDL affects angiogenesis by regulating autophagy and provide a therapeutic target for dHDL-impaired angiogenesis.
      原文链接:
    • 万方数据
    • 维普

    Modeling drug-induced mitochondrial toxicity with human primary cardiomyocytes

    Xiaoli TangHong LiuRongjia RaoYafei Huang...
    301-319页
    查看更多>>摘要：Mitochondrial toxicity induced by therapeutic drugs is a major contributor for cardiotoxicity,posing a serious threat to pharmaceutical industries and patients'lives.However,mitochondrial toxicity testing is not incorporated into routine cardiac safety screening procedures.To accurately model native human cardlomyocytes,we comprehensively evaluated mitochondrial responses of adult human primary car-diomyocytes(hPCMs)to a nucleoside analog,remdesivir(RDV).Comparison of their response to human pluripotent stem cell-derived cardiomyocytes revealed that the latter utilized a mitophagy-based mitochondrial recovery response that was absent in hPCMs.Accordingly,action potential duration was elongated in hPCMs,reflecting clinical incidences of RDV-induced QT prolongation.In a screen for mi-tochondrial protectants,we identified mitochondrial ROS as a primary mediator of RDV-induced cardiotoxicity.Our study demonstrates the utility of hPCMs in the detection of clinically relevant cardiac toxicities,and offers a framework for hPCM-based high-throughput screening of cardioprotective agents.
      原文链接:
    • 万方数据
    • 维普

    Identification and characterization of human hematopoietic mesoderm

    Yuqi WenJingjing ZhaoRunqing ZhangFan Liu...
    320-331页
    查看更多>>摘要：The embryonic mesoderm comprises heterogeneous cell subpopulations with distinct lineage biases.It is unclear whether a bias for the human hematopoietic lineage emerges at this early developmental stage.In this study,we integrated single-cell transcriptomic analyses of human mesoderm cells from embryonic stem cells and embryos,enabling us to identify and define the molecular features of human hematopoietic mesoderm(HM)cells biased towards hematopoietic lineages.We discovered that BMP4 plays an essential role in HM specification and can serve as a marker for HM cells.Mechanistically,BMP4 acts as a downstream target of HDAC1,which modulates the expression of BMP4 by deacetylating its enhancer.Inhibition of HDAC significantly enhances HM specification and promotes subsequent hematopoietic cell differentiation.In conclusion,our study identifies human HM cells and describes new mechanisms for human hema-topoietic development.
      原文链接:
    • 万方数据
    • 维普

    The role of corneal endothelium in macular corneal dystrophy development and recurrence

    Bi-Ning ZhangBenxiang QiChunxiao DongBin Zhang...
    332-344页
    查看更多>>摘要：Macular corneal dystrophy(MCD)is a progressive,bilateral stromal dystrophic disease that arises from mutations in carbohydrate sulfo-transferase 6(CHST6).Corneal transplantation is the ultimate therapeutic solution for MCD patients.Unfortunately,postoperative recur-rence remains a significant challenge.We conducted a retrospective review of a clinical cohort comprising 102 MCD patients with 124 eyes that underwent either penetrating keratoplasty(PKP)or deep anterior lamellar keratoplasty(DALK).Our results revealed that the re-currence rate was nearly three times higher in the DALK group(39.13％,9/23 eyes)compared with the PKP group(10.89％,11/101 eyes),suggesting that surgical replacement of the corneal endothelium for treating MCD is advisable to prevent postoperative recurrence.Our experimental data confirmed the robust mRNA and protein expression of CHST6 in human corneal endothelium and the rodent homolog CHST5 in mouse endothelium.Selective knockdown of wild-type Chst5 in mouse corneal endothelium(ACsiChst5),but not in the corneal stroma,induced experimental MCD with similar extracellular matrix synthesis impairments and corneal thinning as observed in MCD patients.Mice carrying Chst5 point mutation also recapitulated clinical phenotypes of MCD,along with corneal endothelial abnormalities.Intracameral injection of wild-type Chst5 rescued the corneal impairments in ACsiChst5 mice and retarded the disease progression in Chst5 mutant mice.Overall,our study provides new mechanistic insights and therapeutic approaches for MCD treatment by highlighting the role of corneal endothelium in MCD development.
      原文链接:
    • 万方数据
    • 维普

    STING signaling in islet macrophages impairs insulin secretion in obesity

    Ze HongSaihua ChenJing SunDan Cheng...
    345-359页
    查看更多>>摘要：The innate immune regulator stimulator of interferon genes(STING)mediates self-DNA sensing and leads to the induction of type Ⅰinterferons and inflammatory cytokines,which promotes the progression of various inflammatory and autoimmune diseases.Innate im-mune system plays a critical role in regulating obesity-induced islet dysfunction,whereas the potential effect of STING signaling is not fully understood.Here,we demonstrate that STING is mainly expressed and activated in islet macrophages upon high-fat diet(HFD)feeding.Sting-/-alleviates HFD-induced islet inflammation by inhibiting the expression of pro-inflammatory cytokines and the infiltration of macrophages.Mechanically,palmitic acid incubation promotes mitochondrial DNA leakage into the cytosol and subsequently activates STING pathway in macrophages.Additionally,STING activation in macrophages impairs glucose-stimulated insulin secretion by mediating the engulfment of β cell insulin secretory granules.Pharmacologically inhibiting STING activation enhances insulin secretion to control hyperglycemia.Together,our results reveal a regulatory mechanism in controlling the islet inflammation and insulin secretion in diet-induced obesity and suggest that selective blocking of the STING activation may be a promising strategy for treating type 2 diabetes.
      原文链接:
    • 万方数据
    • 维普

    Melatonin decreases GSDME mediated mesothelial cell pyrop-tosis and prevents peritoneal fibrosis and ultrafiltration failure

    Hongxia RuanXuejuan LiLina ZhouZihan Zheng...
    360-378页
    查看更多>>摘要：Peritoneal fibrosis together with increased capillaries is the primary cause of peritoneal dialysis failure.Mesothelial cell loss is an initiating event for peritoneal fibrosis.We find that the elevated glucose concentrations in peritoneal dialysate drive mesothelial cell pyroptosis in a manner dependent on caspase-3 and Gasdermin E,driving downstream inflammatory responses,including the activation of macrophages.Moreover,pyroptosis is associated with elevated vascular endothelial growth factor A and C,two key factors in vascular angiogenesis and lymphatic vessel formation.GSDME deficiency mice are protected from high glucose induced peritoneal fibrosis and ultrafiltration failure.Application of melatonin abrogates mesothelial cell pyroptosis through a MT1R-mediated action,and successfully reduces peritoneal fibrosis and angiogenesis in an animal model while preserving dialysis efficacy.Mechanistically,melatonin treatment maintains mi-tochondrial integrity in mesothelial cells,meanwhile activating mTOR signaling through an increase in the glycolysis product dihydrox-yacetone phosphate.These effects together with quenching free radicals by melatonin help mesothelial cells maintain a relatively stable internal environment in the face of high-glucose stress.Thus,Melatonin treatment holds some promise in preserving mesothelium integrity and in decreasing angiogenesis to protect peritoneum function in patients undergoing peritoneal dialysis.
      原文链接:
    • 万方数据