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  1. Article ; Online: Cell-cell communication in kidney fibrosis.

    He, Meizhi / Liu, Zhao / Li, Li / Liu, Youhua

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

    2023  Volume 39, Issue 5, Page(s) 761–769

    Abstract: Kidney fibrosis is a common outcome of a wide variety of chronic kidney diseases, in which virtually all kinds of renal resident and infiltrating cells are involved. As such, well-orchestrated intercellular communication is of vital importance in ... ...

    Abstract Kidney fibrosis is a common outcome of a wide variety of chronic kidney diseases, in which virtually all kinds of renal resident and infiltrating cells are involved. As such, well-orchestrated intercellular communication is of vital importance in coordinating complex actions during renal fibrogenesis. Cell-cell communication in multicellular organisms is traditionally assumed to be mediated by direct cell contact or soluble factors, including growth factors, cytokines and chemokines, through autocrine, paracrine, endocrine and juxtacrine signaling mechanisms. Growing evidence also demonstrates that extracellular vesicles, lipid bilayer-encircled particles naturally released from almost all types of cells, can act as a vehicle to transfer a diverse array of biomolecules including proteins, mRNA, miRNA and lipids to mediate cell-cell communication. We recently described a new mode of intercellular communication via building a special extracellular niche by insoluble matricellular proteins. Kidney cells, upon injury, produce and secrete different matricellular proteins, which incorporate into the local extracellular matrix network, and regulate the behavior, trajectory and fate of neighboring cells in a spatially confined fashion. This extracellular niche-mediated cell-cell communication is unique in that it restrains the crosstalk between cells within a particular locality. Detailed delineation of this unique manner of intercellular communication will help to elucidate the mechanism of kidney fibrosis and could offer novel insights in developing therapeutic intervention.
    MeSH term(s) Cell Communication ; Humans ; Fibrosis ; Animals ; Kidney Diseases/pathology ; Kidney Diseases/metabolism ; Kidney Diseases/etiology ; Kidney/pathology ; Kidney/metabolism
    Language English
    Publishing date 2023-11-30
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 90594-x
    ISSN 1460-2385 ; 0931-0509
    ISSN (online) 1460-2385
    ISSN 0931-0509
    DOI 10.1093/ndt/gfad257
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2198: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 329: Show issues

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  2. Article ; Online: Proteomic landscape of the extracellular matrix in the fibrotic kidney.

    Li, Li / He, Meizhi / Tang, Xiaoman / Huang, Junxin / Li, Jing / Hong, Xue / Fu, Haiyan / Liu, Youhua

    Kidney international

    2023  Volume 103, Issue 6, Page(s) 1063–1076

    Abstract: The extracellular matrix (ECM) is a complex three-dimensional network of proteins surrounding cells, forming a niche that controls cell adhesion, proliferation, migration and differentiation. The ECM network provides an architectural scaffold for ... ...

    Abstract The extracellular matrix (ECM) is a complex three-dimensional network of proteins surrounding cells, forming a niche that controls cell adhesion, proliferation, migration and differentiation. The ECM network provides an architectural scaffold for surrounding cells and undergoes dynamic changes in composition and contents during the evolution of chronic kidney disease (CKD). Here, we unveiled the proteomic landscape of the ECM by delineating proteome-wide and ECM-specific alterations in normal and fibrotic kidneys. Decellularized kidney tissue scaffolds were made and subjected to proteomic profiling by liquid chromatography with tandem mass spectrometry. A total of 172 differentially expressed proteins were identified in these scaffolds from mice with CKD. Through bioinformatics analysis and experimental validation, we identified a core set of nine signature proteins, which could play a role in establishing an oxidatively stressed, profibrotic, proinflammatory and antiangiogenetic microenvironment. Among these nine proteins, glutathione peroxidase 3 (GPX3) was the only protein with downregulated expression during CKD. Knockdown of GPX3 in vivo augmented ECM expression and aggravated kidney fibrotic lesions after obstructive injury. Transcriptomic profiling revealed that GPX3 depletion resulted in an altered expression of the genes enriched in hypoxia pathway. Knockdown of GPX3 induced NADPH oxidase 2 expression, promoted kidney generation of reactive oxygen species and activated p38 mitogen-activated protein kinase. Conversely, overexpression of exogenous GPX3 alleviated kidney fibrosis, inhibited NADPH oxidase 2 and p38 mitogen-activated protein kinase. These findings suggest that oxidative stress is a pivotal element of the fibrogenic microenvironment. Thus, our studies represent a comprehensive proteomic characterization of the ECM in the fibrotic kidney and provide novel insights into molecular composition of the fibrogenic microenvironment.
    MeSH term(s) Mice ; Animals ; NADPH Oxidase 2/metabolism ; Proteomics ; Extracellular Matrix/metabolism ; Fibrosis ; Kidney/pathology ; Renal Insufficiency, Chronic/pathology ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism
    Chemical Substances NADPH Oxidase 2 (EC 1.6.3.-) ; Extracellular Matrix Proteins
    Language English
    Publishing date 2023-02-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2023.01.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 797: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article: The relationship between pancreatic cancer and type 2 diabetes: cause and consequence.

    Li, Yan / Bian, Xiaohui / Wei, Shuyi / He, Meizhi / Yang, Yuelian

    Cancer management and research

    2019  Volume 11, Page(s) 8257–8268

    Abstract: Pancreatic cancer (PC) is a devastating and lethal malignant disease and it is well known that there is a complex bidirectional relationship between PC and type 2 diabetes mellitus (T2DM). In order to more deeply summarize the relationship between them, ... ...

    Abstract Pancreatic cancer (PC) is a devastating and lethal malignant disease and it is well known that there is a complex bidirectional relationship between PC and type 2 diabetes mellitus (T2DM). In order to more deeply summarize the relationship between them, this article summarizes the epidemiological data on the relationship between PC and T2DM in the past 5 years, and further explains the mechanism of interaction between them. Meanwhile, it also summed up the effects of drug therapy for T2DM on PC and the impact of T2DM on surgical resection of PC. Epidemiological studies clearly indicate that the risk of PC is increased in patients with T2DM. But increasing epidemiological data points out that PC also acts as a cause of T2DM and new-onset T2DM is sign and consequence of PC. Insulin resistance, hyperinsulinemia, hyperglycemia, and chronic inflammation are the mechanisms of T2DM-Associated PC. Metformin decreases the risk of PC, while insulin therapy increases the risk of PC. Besides, studies have shown that T2DM decreases the survival in patients with PC resection.
    Language English
    Publishing date 2019-09-09
    Publishing country New Zealand
    Document type Journal Article ; Review
    ZDB-ID 2508013-1
    ISSN 1179-1322
    ISSN 1179-1322
    DOI 10.2147/CMAR.S211972
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Oxidatively stressed extracellular microenvironment drives fibroblast activation and kidney fibrosis.

    Li, Li / Lu, Meizhi / Peng, Yiling / Huang, Junxin / Tang, Xiaoman / Chen, Jian / Li, Jing / Hong, Xue / He, Meizhi / Fu, Haiyan / Liu, Ruiyuan / Hou, Fan Fan / Zhou, Lili / Liu, Youhua

    Redox biology

    2023  Volume 67, Page(s) 102868

    Abstract: Kidney fibrosis is associated with tubular injury, oxidative stress and activation of interstitial fibroblasts. However, whether these events are somehow connected is poorly understood. In this study, we show that glutathione peroxidase-3 (GPX3) ... ...

    Abstract Kidney fibrosis is associated with tubular injury, oxidative stress and activation of interstitial fibroblasts. However, whether these events are somehow connected is poorly understood. In this study, we show that glutathione peroxidase-3 (GPX3) depletion in renal tubular epithelium after kidney injury plays a central role in orchestrating an oxidatively stressed extracellular microenvironment, which drives interstitial fibroblast activation and proliferation. Through transcriptional profiling by RNA-sequencing, we found that the expression of GPX3 was down-regulated in various models of chronic kidney disease (CKD), which was correlated with induction of nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase-4 (NOX4). By using decellularized extracellular matrix (ECM) scaffold, we demonstrated that GPX3-depleted extracellular microenvironment spontaneously induced NOX4 expression and reactive oxygen species (ROS) production in renal fibroblasts and triggered their activation and proliferation. Activation of NOX4 by advanced oxidation protein products (AOPPs) mimicked the loss of GPX3, increased the production of ROS, stimulated fibroblast activation and proliferation, and activated protein kinase C-α (PKCα)/mitogen-activated protein kinase (MAPK)/signal transducer and activator of transcription 3 (STAT3) signaling. Silencing NOX4 or inhibition of MAPK with small molecule inhibitors hampered fibroblast activation and proliferation. In mouse model of CKD, knockdown of NOX4 repressed renal fibroblast activation and proliferation and alleviated kidney fibrosis. These results indicate that loss of GPX3 orchestrates an oxidatively stressed extracellular microenvironment, which promotes fibroblast activation and proliferation through a cascade of signal transduction. Our studies underscore the crucial role of extracellular microenvironment in driving fibroblast activation and kidney fibrosis.
    MeSH term(s) Mice ; Animals ; Reactive Oxygen Species/metabolism ; Kidney/metabolism ; Renal Insufficiency, Chronic/metabolism ; Fibroblasts/metabolism ; NADPH Oxidase 4/genetics ; NADPH Oxidase 4/metabolism ; Fibrosis
    Chemical Substances Reactive Oxygen Species ; NADPH Oxidase 4 (EC 1.6.3.-)
    Language English
    Publishing date 2023-09-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2023.102868
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The Clinicopathologic and Prognostic Significance of Programmed Cell Death Ligand 1 (PD-L1) Expression in Patients With Prostate Cancer: A Systematic Review and Meta-Analysis.

    Li, Yan / Huang, Qingying / Zhou, Yaoyao / He, Meizhi / Chen, Jianhong / Gao, Yubo / Wang, Xue

    Frontiers in pharmacology

    2019  Volume 9, Page(s) 1494

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2019-01-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2018.01494
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Nomograms to predict overall survival and cancer-specific survival in patients with adrenocortical carcinoma.

    Li, Yan / Bian, Xiaohui / Ouyang, Junyu / Wei, Shuyi / He, Meizhi / Luo, Zelong

    Cancer management and research

    2018  Volume 10, Page(s) 6949–6959

    Abstract: Purpose: To develop nomogram models to predict individualized estimates of overall survival (OS) and cancer-specific survival (CSS) in patients with adrenocortical carcinoma (ACC).: Patients and methods: A total of 751 patients with ACC were ... ...

    Abstract Purpose: To develop nomogram models to predict individualized estimates of overall survival (OS) and cancer-specific survival (CSS) in patients with adrenocortical carcinoma (ACC).
    Patients and methods: A total of 751 patients with ACC were identified within the Surveillance Epidemiology, and End Results (SEER) database between 1973 and 2015. The predictors comprised marital status, sex, age at diagnosis, year of diagnosis, laterality, histologic grade, ethnicity, historic stage, radiation therapy, chemotherapy, and surgery of primary site. Based on the results of the multivariate logistic regression analyses, the nomogram models were used for predicting OS and CSS in patients with ACC. The nomograms were tested using concordance index (C-index) and calibration curves.
    Results: In univariate and multivariate analyses of OS, OS was significantly associated with age at diagnosis, year of diagnosis, histologic grade, historic stage, and chemotherapy. In univariate and multivariate analyses of CSS, age at diagnosis, year of diagnosis, historic stage, and chemotherapy were the independent risk factors with CSS. These characteristics were included in the nomograms predicting OS and CSS. The nomograms demonstrated good accuracy in predicting OS and CSS, with the C-index of 0.677 and 0.672.
    Conclusion: These clinically useful tools predicted OS and CSS in patients with ACC using readily available clinicopathologic factors and could aid individualized clinical decision making.
    Language English
    Publishing date 2018-12-13
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2508013-1
    ISSN 1179-1322
    ISSN 1179-1322
    DOI 10.2147/CMAR.S187169
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: The Prognostic and Clinicopathological Roles of PD-L1 Expression in Colorectal Cancer: A Systematic Review and Meta-Analysis.

    Li, Yan / He, Meizhi / Zhou, Yaoyao / Yang, Chen / Wei, Shuyi / Bian, Xiaohui / Christopher, Odong / Xie, Lang

    Frontiers in pharmacology

    2019  Volume 10, Page(s) 139

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2019-02-28
    Publishing country Switzerland
    Document type Systematic Review
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2019.00139
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: The Efficacy of Different Chemotherapy Regimens for Advanced Biliary Tract Cancer: A Systematic Review and Network Meta-Analysis.

    Li, Yan / Zhou, Yaoyao / Hong, Yonglan / He, Meizhi / Wei, Shuyi / Yang, Chen / Zheng, Dayong / Liu, Feiye

    Frontiers in oncology

    2019  Volume 9, Page(s) 441

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2019-05-29
    Publishing country Switzerland
    Document type Systematic Review
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2019.00441
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Artificial liver research output and citations from 2004 to 2017: a bibliometric analysis.

    Li, Yan / He, Meizhi / Zou, Ziyuan / Bian, Xiaohui / Huang, Xiaowen / Yang, Chen / Wei, Shuyi / Dai, Shixue

    PeerJ

    2019  Volume 6, Page(s) e6178

    Abstract: Background: Researches on artificial livers greatly contribute to the clinical treatments for liver failure. This study aimed to evaluate the research output of artificial livers and citations from 2004 to 2017 through a bibliometric analysis.: ... ...

    Abstract Background: Researches on artificial livers greatly contribute to the clinical treatments for liver failure. This study aimed to evaluate the research output of artificial livers and citations from 2004 to 2017 through a bibliometric analysis.
    Methods: A list of included articles on artificial livers were generated after a comprehensive search of the Web of Science Core Collection (from 2004 to 2017) with the following basic information: number of publications, citations, publication year, country of origin, authors and authorship, funding source, journals, institutions, keywords, and research area.
    Results: A total of 968 included articles ranged from 47 citations to 394 citations with a fluctuation. The publications were distributed in 12 countries, led by China (
    Discussion: This study shows the process and tendency of artificial liver research with a comprehensive analysis on artificial livers. However, although it seems that the future of artificial livers seems brighter for hepatocyte transplantation, the systems of artificial livers now are inclined on focusing on blood purification, plasma exchange, etc.
    Language English
    Publishing date 2019-01-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2703241-3
    ISSN 2167-8359
    ISSN 2167-8359
    DOI 10.7717/peerj.6178
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Fibrillin-1-enriched microenvironment drives endothelial injury and vascular rarefaction in chronic kidney disease.

    Li, Li / Liao, Jinlin / Yuan, Qian / Hong, Xue / Li, Jing / Peng, Yiling / He, Meizhi / Zhu, Haili / Zhu, Mingsheng / Hou, Fan Fan / Fu, Haiyan / Liu, Youhua

    Science advances

    2021  Volume 7, Issue 5

    Abstract: Endothelial cell injury leading to microvascular rarefaction is a characteristic feature of chronic kidney disease (CKD). However, the mechanism underlying endothelial cell dropout is poorly defined. Here, we show a central role of the extracellular ... ...

    Abstract Endothelial cell injury leading to microvascular rarefaction is a characteristic feature of chronic kidney disease (CKD). However, the mechanism underlying endothelial cell dropout is poorly defined. Here, we show a central role of the extracellular microenvironment in controlling endothelial cell survival and proliferation in CKD. When cultured on a decellularized kidney tissue scaffold (KTS) from fibrotic kidney, endothelial cells increased the expression of proapoptotic proteins. Proteomics profiling identified fibrillin-1 (FBN1) as a key component of the fibrotic KTS, which was up-regulated in animal models and patients with CKD. FBN1 induced apoptosis of endothelial cells and inhibited their proliferation in vitro. RNA sequencing uncovered activated integrin α
    MeSH term(s) Animals ; Cellular Microenvironment/genetics ; Cellular Microenvironment/physiology ; Endothelial Cells/metabolism ; Female ; Fibrillin-1/genetics ; Fibrillin-1/metabolism ; Fibrosis ; Humans ; Kidney/pathology ; Male ; Mice ; Microvascular Rarefaction/metabolism ; Microvascular Rarefaction/pathology ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/pathology
    Chemical Substances Fibrillin-1
    Language English
    Publishing date 2021-01-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abc7170
    Database MEDical Literature Analysis and Retrieval System OnLINE

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