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  1. Artikel ; Online: Involvement of gut microbiota recovery and autophagy induction in Youhua Kuijie Formula's protection against experimental ulcerative colitis.

    Sheng, Tianjiao / Wang, Lei / Yan, Simeng / Wei, Qiuyu / Geng, Xiao / Lan, Weiru / Chen, Yan / Liu, Yuedong / Li, Na

    Experimental animals

    2024  

    Abstract: ... mucosal barrier and disrupted gut microbiota. Youhua Kuijie formula is a classic empirical prescription ... of Youhua Kuijie Formula on DSS-induced UC in mice and uncover the related mechanism. Youhua Kuijie Formula ... The protective effect of Youhua Kuijie Formula was evidenced by reduced pathological symptoms accompanied by palliative ...

    Abstract Ulcerative colitis (UC) is characterized by overactive inflammatory response, impaired intestinal mucosal barrier and disrupted gut microbiota. Youhua Kuijie formula is a classic empirical prescription based on the pathogenesis of UC. The present study was designed to verify the protective effect of Youhua Kuijie Formula on DSS-induced UC in mice and uncover the related mechanism. Youhua Kuijie Formula were orally administrated to UC mice induced by DSS dissolved in drinking water for ten days. The protective effect of Youhua Kuijie Formula was evidenced by reduced pathological symptoms accompanied by palliative inflammatory response and relatively intact intestinal barrier. The data from 16S rRNA gene sequencing and GC-MS untargeted metabolomics indicated that the supplement of Youhua Kuijie Formula restructured gut microbiota community structure, and thereby modulated the metabolic profiles in UC mice. The analysis of pathway enrichment analysis suggested the major alterations in metabolic pathway were related to protein digestion and absorption. Besides, the results of the following experiments suggested that Youhua Kuijie Formula treatment increased adenosine monophosphate-activated protein kinase (AMPK) activation, decreased mechanistic target of rapamycin (mTOR) phosphorylation, and thereby reversing autophagy deficiency in the intestinal tract of UC mice. Collectively, our results demonstrated that the regulation of AMPK/mTOR was involved in Youhua Kuijie Formula administration mediated protective effect on UC.
    Sprache Englisch
    Erscheinungsdatum 2024-04-09
    Erscheinungsland Japan
    Dokumenttyp Journal Article
    ZDB-ID 2088228-2
    ISSN 1881-7122 ; 1341-1357 ; 0007-5124
    ISSN (online) 1881-7122
    ISSN 1341-1357 ; 0007-5124
    DOI 10.1538/expanim.23-0166
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Buch ; Online: Medicinal Plants for Cardiovascular and Neurodegenerative Aging-related Diseases: From Bench to Bedside

    Liu, Yue / Echeverria Moran, Valentina / Xu, Youhua / Xu, Youhua

    2020  

    Schlagwörter Science: general issues ; Pharmacology ; medicinal plants ; aging ; age-related diseases ; cardiovascular disease ; neurodegenerative diseases
    Umfang 1 electronic resource (294 pages)
    Verlag Frontiers Media SA
    Dokumenttyp Buch ; Online
    Anmerkung English ; Open Access
    HBZ-ID HT021230427
    ISBN 9782889661602 ; 2889661601
    Datenquelle ZB MED Katalog Medizin, Gesundheit, Ernährung, Umwelt, Agrar

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  3. Artikel: The extracellular matrix glycoprotein fibrillin-1 in health and disease.

    Li, Li / Huang, Junxin / Liu, Youhua

    Frontiers in cell and developmental biology

    2024  Band 11, Seite(n) 1302285

    Abstract: Fibrillin-1 (FBN1) is a large, cysteine-rich, calcium binding extracellular matrix glycoprotein encoded ... ...

    Abstract Fibrillin-1 (FBN1) is a large, cysteine-rich, calcium binding extracellular matrix glycoprotein encoded by
    Sprache Englisch
    Erscheinungsdatum 2024-01-10
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2023.1302285
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Animal Models of Type 2 Diabetes Complications: A Review.

    Sun, Zhongyan / Liu, Yadi / Zhao, Yonghua / Xu, Youhua

    Endocrine research

    2024  Band 49, Heft 1, Seite(n) 46–58

    Abstract: Diabetes mellitus is a multifactorial metabolic disease, of which type 2 diabetes (T2D) is one of the most common. The complications of diabetes are far more harmful than diabetes itself. Type 2 diabetes complications include diabetic nephropathy (DN), ... ...

    Abstract Diabetes mellitus is a multifactorial metabolic disease, of which type 2 diabetes (T2D) is one of the most common. The complications of diabetes are far more harmful than diabetes itself. Type 2 diabetes complications include diabetic nephropathy (DN), diabetic heart disease, diabetic foot ulcers (DFU), diabetic peripheral neuropathy (DPN), and diabetic retinopathy (DR)
    Mesh-Begriff(e) Animals ; Diabetes Mellitus, Type 2/complications ; Diabetic Foot/complications ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Diabetic Neuropathies/etiology ; Diabetic Neuropathies/metabolism ; Diabetic Neuropathies/pathology ; Models, Animal ; Risk Factors
    Sprache Englisch
    Erscheinungsdatum 2024-01-04
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 605823-1
    ISSN 1532-4206 ; 0743-5800
    ISSN (online) 1532-4206
    ISSN 0743-5800
    DOI 10.1080/07435800.2023.2278049
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1273: Hefte anzeigen Standort:
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  5. Artikel ; Online: The extracellular matrix glycoprotein fibrillin-1 in health and disease

    Li Li / Junxin Huang / Youhua Liu

    Frontiers in Cell and Developmental Biology, Vol

    2024  Band 11

    Abstract: Fibrillin-1 (FBN1) is a large, cysteine-rich, calcium binding extracellular matrix glycoprotein encoded by FBN1 gene. It serves as a structural component of microfibrils and provides force-bearing mechanical support in elastic and nonelastic connective ... ...

    Abstract Fibrillin-1 (FBN1) is a large, cysteine-rich, calcium binding extracellular matrix glycoprotein encoded by FBN1 gene. It serves as a structural component of microfibrils and provides force-bearing mechanical support in elastic and nonelastic connective tissue. As such, mutations in the FBN1 gene can cause a wide variety of genetic diseases such as Marfan syndrome, an autosomal dominant disorder characterized by ocular, skeletal and cardiovascular abnormalities. FBN1 also interacts with numerous microfibril-associated proteins, growth factors and cell membrane receptors, thereby mediating a wide range of biological processes such as cell survival, proliferation, migration and differentiation. Dysregulation of FBN1 is involved in the pathogenesis of many human diseases, such as cancers, cardiovascular disorders and kidney diseases. Paradoxically, both depletion and overexpression of FBN1 upregulate the bioavailability and signal transduction of TGF-β via distinct mechanisms in different settings. In this review, we summarize the structure and expression of FBN1 and present our current understanding of the functional role of FBN1 in various human diseases. This knowledge will allow to develop better strategies for therapeutic intervention of FBN1 related diseases.
    Schlagwörter FBN1 ; extracellular matrix ; marfan syndrome ; TGF-β ; chronic kidney diseases ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2024-01-01T00:00:00Z
    Verlag Frontiers Media S.A.
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Animal Models of Kidney Disease: Challenges and Perspectives.

    Liang, Jianqing / Liu, Youhua

    Kidney360

    2023  Band 4, Heft 10, Seite(n) 1479–1493

    Abstract: Kidney disease is highly prevalent and affects approximately 850 million people worldwide. It is also associated with high morbidity and mortality, and current therapies are incurable and often ineffective. Animal models are indispensable for ... ...

    Abstract Kidney disease is highly prevalent and affects approximately 850 million people worldwide. It is also associated with high morbidity and mortality, and current therapies are incurable and often ineffective. Animal models are indispensable for understanding the pathophysiology of various kidney diseases and for preclinically testing novel remedies. In the last two decades, rodents continue to be the most used models for imitating human kidney diseases, largely because of the increasing availability of many unique genetically modified mice. Despite many limitations and pitfalls, animal models play an essential and irreplaceable role in gaining novel insights into the mechanisms, pathologies, and therapeutic targets of kidney disease. In this review, we highlight commonly used animal models of kidney diseases by focusing on experimental AKI, CKD, and diabetic kidney disease. We briefly summarize the pathological characteristics, advantages, and drawbacks of some widely used models. Emerging animal models such as mini pig, salamander, zebrafish, and drosophila, as well as human-derived kidney organoids and kidney-on-a-chip are also discussed. Undoubtedly, careful selection and utilization of appropriate animal models is of vital importance in deciphering the mechanisms underlying nephropathies and evaluating the efficacy of new treatment options. Such studies will provide a solid foundation for future diagnosis, prevention, and treatment of human kidney diseases.
    Mesh-Begriff(e) Swine ; Animals ; Mice ; Humans ; Zebrafish ; Swine, Miniature ; Kidney/pathology ; Models, Animal ; Diabetic Nephropathies ; Rodentia ; Drosophila
    Sprache Englisch
    Erscheinungsdatum 2023-08-01
    Erscheinungsland United States
    Dokumenttyp Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2641-7650
    ISSN (online) 2641-7650
    DOI 10.34067/KID.0000000000000227
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: Klotho-derived peptide KP1 ameliorates SARS-CoV-2-associated acute kidney injury.

    Xu, Jie / Lin, Enqing / Hong, Xue / Li, Li / Gu, Jun / Zhao, Jinghong / Liu, Youhua

    Frontiers in pharmacology

    2024  Band 14, Seite(n) 1333389

    Abstract: Introduction: ...

    Abstract Introduction:
    Sprache Englisch
    Erscheinungsdatum 2024-01-03
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2023.1333389
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Commercial genetically modified corn and soybean are poised following pilot planting in China.

    Sun, Mei / Li, Suzhen / Yang, Wenzhu / Zhao, Bowen / Wang, Youhua / Liu, Xiaoqing

    Molecular plant

    2024  Band 17, Heft 4, Seite(n) 519–521

    Mesh-Begriff(e) Glycine max/genetics ; Zea mays/genetics ; Agriculture ; China ; Plants, Genetically Modified/genetics
    Sprache Englisch
    Erscheinungsdatum 2024-03-07
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2393618-6
    ISSN 1752-9867 ; 1674-2052
    ISSN (online) 1752-9867
    ISSN 1674-2052
    DOI 10.1016/j.molp.2024.03.005
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Matrix Metalloproteinase-10 in Kidney Injury Repair and Disease

    Xiaoli Sun / Youhua Liu

    International Journal of Molecular Sciences, Vol 23, Iss 2131, p

    2022  Band 2131

    Abstract: Matrix metalloproteinase-10 (MMP-10) is a zinc-dependent endopeptidase with the ability to degrade a broad spectrum of extracellular matrices and other protein substrates. The expression of MMP-10 is induced in acute kidney injury (AKI) and chronic ... ...

    Abstract Matrix metalloproteinase-10 (MMP-10) is a zinc-dependent endopeptidase with the ability to degrade a broad spectrum of extracellular matrices and other protein substrates. The expression of MMP-10 is induced in acute kidney injury (AKI) and chronic kidney disease (CKD), as well as in renal cell carcinoma (RCC). During the different stages of kidney injury, MMP-10 may exert distinct functions by cleaving various bioactive substrates including heparin-binding epidermal growth factor (HB-EGF), zonula occludens-1 (ZO-1), and pro-MMP-1, -7, -8, -9, -10, -13. Functionally, MMP-10 is reno-protective in AKI by promoting HB-EGF-mediated tubular repair and regeneration, whereas it aggravates podocyte dysfunction and proteinuria by disrupting glomerular filtration integrity via degrading ZO-1. MMP-10 is also involved in cancerous invasion and emerges as a promising therapeutic target in patients with RCC. As a secreted protein, MMP-10 could be detected in the circulation and presents an inverse correlation with renal function. Due to the structural similarities between MMP-10 and the other MMPs, development of specific inhibitors targeting MMP-10 is challenging. In this review, we summarize our current understanding of the role of MMP-10 in kidney diseases and discuss the potential mechanisms of its actions.
    Schlagwörter MMP-10 ; acute kidney injury ; chronic kidney disease ; renal fibrosis ; proteinuria ; HB-EGF ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2022-02-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; 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  Band 39, Heft 5, Seite(n) 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-Begriff(e) Cell Communication ; Humans ; Fibrosis ; Animals ; Kidney Diseases/pathology ; Kidney Diseases/metabolism ; Kidney Diseases/etiology ; Kidney/pathology ; Kidney/metabolism
    Sprache Englisch
    Erscheinungsdatum 2023-11-30
    Erscheinungsland England
    Dokumenttyp 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
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    Zs.MO 329: Hefte anzeigen

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