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  1. Book ; Thesis: Perivaskuläre Progenitorzellen in Organfibrose und vaskulärer Kalzifikation

    Kramann, Rafael

    2018  

    Author's details vorgelegt von Universitätsprofessor Dr. med. Rafael Kramann
    Language German ; English
    Size [ca. 160] verschieden gezählte Blätter, Illustrationen
    Publishing place Aachen
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Habilitationsschrift, Rheinisch-Westfälische Technische Hochschule Aachen, 2018
    Note Die Habilitationsschrift besteht aus einem Text und 7 Aufsätzen teils in englischer Sprache
    HBZ-ID HT019763110
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2018 E 1091 order for loan Magazin

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  2. Article ; Online: A spatially resolved atlas of healthy and injured kidney cell states.

    Kuppe, Christoph / Kramann, Rafael

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

    2023  Volume 39, Issue 3, Page(s) 379–381

    MeSH term(s) Humans ; Kidney ; Epithelial Cells
    Language English
    Publishing date 2023-07-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 90594-x
    ISSN 1460-2385 ; 0931-0509
    ISSN (online) 1460-2385
    ISSN 0931-0509
    DOI 10.1093/ndt/gfad203
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Metabolic reprogramming heterogeneity in chronic kidney disease.

    Miguel, Verónica / Kramann, Rafael

    FEBS open bio

    2023  Volume 13, Issue 7, Page(s) 1154–1163

    Abstract: Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and ... ...

    Abstract Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and immune cells. Emerging evidence suggests that alterations in metabolism are not only a feature of but also play an influential role in the pathogenesis of renal fibrosis. The application of omics technologies to cell-tracing animal models and follow-up functional data suggest that cell-type-specific metabolic shifts have particular roles in the fibrogenic response. In this review, we cover the main metabolic reprogramming outcomes in renal fibrosis and provide a future perspective on the field of renal fibrometabolism.
    MeSH term(s) Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Renal Insufficiency, Chronic/physiopathology ; Fibrosis/complications ; Fibrosis/metabolism ; Fibrosis/pathology ; Fibrosis/physiopathology ; Humans ; Animals ; Oxidative Phosphorylation ; Glucose/metabolism ; Glutamine/metabolism ; Fatty Acids/metabolism
    Chemical Substances Glucose (IY9XDZ35W2) ; Glutamine (0RH81L854J) ; Fatty Acids
    Language English
    Publishing date 2023-02-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13568
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mechanisms of kidney fibrosis and routes towards therapy.

    Yamashita, Noriyuki / Kramann, Rafael

    Trends in endocrinology and metabolism: TEM

    2023  Volume 35, Issue 1, Page(s) 31–48

    Abstract: Kidney fibrosis is the final common pathway of virtually all chronic kidney diseases (CKDs) and is therefore considered to be a promising therapeutic target for these conditions. However, despite great progress in recent years, no targeted antifibrotic ... ...

    Abstract Kidney fibrosis is the final common pathway of virtually all chronic kidney diseases (CKDs) and is therefore considered to be a promising therapeutic target for these conditions. However, despite great progress in recent years, no targeted antifibrotic therapies for the kidney have been approved, likely because the complex mechanisms that initiate and drive fibrosis are not yet completely understood. Recent single-cell genomic approaches have allowed novel insights into kidney fibrosis mechanisms in mouse and human, particularly the heterogeneity and differentiation processes of myofibroblasts, the role of injured epithelial cells and immune cells, and their crosstalk mechanisms. In this review we summarize the key mechanisms that drive kidney fibrosis, including recent advances in understanding the mechanisms, as well as potential routes for developing novel targeted antifibrotic therapeutics.
    MeSH term(s) Humans ; Mice ; Animals ; Kidney/pathology ; Fibrosis ; Renal Insufficiency, Chronic ; Myofibroblasts/pathology ; Epithelial Cells
    Language English
    Publishing date 2023-09-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2023.09.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Metabolic reprogramming heterogeneity in chronic kidney disease

    Miguel, Verónica / Kramann, Rafael

    FEBS Open Bio. 2023 July, v. 13, no. 7 p.1154-1163

    2023  

    Abstract: Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and ... ...

    Abstract Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and immune cells. Emerging evidence suggests that alterations in metabolism are not only a feature of but also play an influential role in the pathogenesis of renal fibrosis. The application of omics technologies to cell‐tracing animal models and follow‐up functional data suggest that cell‐type‐specific metabolic shifts have particular roles in the fibrogenic response. In this review, we cover the main metabolic reprogramming outcomes in renal fibrosis and provide a future perspective on the field of renal fibrometabolism.
    Keywords animals ; extracellular matrix ; fibrosis ; kidney diseases ; metabolism ; pathogenesis
    Language English
    Dates of publication 2023-07
    Size p. 1154-1163.
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    ZDB-ID 2651702-4
    ISSN 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13568
    Database NAL-Catalogue (AGRICOLA)

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  6. Article ; Online: Mapping the human kidney using single-cell genomics.

    Schreibing, Felix / Kramann, Rafael

    Nature reviews. Nephrology

    2022  Volume 18, Issue 6, Page(s) 347–360

    Abstract: The field of single-cell genomics and spatial technologies is rapidly evolving and has already provided unprecedented insights into complex tissues. Major advances have been made in dissecting the cellular composition and spatiotemporal interactions that ...

    Abstract The field of single-cell genomics and spatial technologies is rapidly evolving and has already provided unprecedented insights into complex tissues. Major advances have been made in dissecting the cellular composition and spatiotemporal interactions that mediate developmental processes in the fetal kidney. Single-cell technologies have also provided detailed insights into the heterogeneity of cell types within the healthy adult and shed light on the complex cellular mechanisms that contribute to kidney disease. The in-depth characterization of specific cell types associated with acute kidney injury and glomerular diseases has potential for the development of prognostic biomarkers and new therapeutics. Analyses of pathway activity in clear-cell renal cell carcinoma can predict the sensitivity of tumour cells to specific inhibitors. The identification of the cell of origin of renal cell carcinoma and of new cell types within the tumour microenvironment also has implications for the development of targeted therapeutics. Similarly, single-cell sequencing has provided new insights into the mechanisms underlying kidney fibrosis, specifically our understanding of myofibroblast origins and the contribution of cell crosstalk within the fibrotic niche to disease progression. These and future studies will enable the creation of a map to aid our understanding of the cellular processes and interactions in the developing, healthy and diseased kidney.
    MeSH term(s) Carcinoma, Renal Cell/pathology ; Fibrosis ; Genomics ; Humans ; Kidney/pathology ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; Tumor Microenvironment/genetics
    Language English
    Publishing date 2022-03-17
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-022-00553-4
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  7. Article ; Online: Multiomic Spatial Mapping of Myocardial Infarction and Implications for Personalized Therapy.

    Schumacher, David / Kramann, Rafael

    Arteriosclerosis, thrombosis, and vascular biology

    2022  Volume 43, Issue 2, Page(s) 192–202

    Abstract: Ischemic heart disease including myocardial infarction is still the leading cause of death worldwide. Although the survival early after myocardial infarction has been significantly improved by the introduction of percutaneous coronary intervention, long- ... ...

    Abstract Ischemic heart disease including myocardial infarction is still the leading cause of death worldwide. Although the survival early after myocardial infarction has been significantly improved by the introduction of percutaneous coronary intervention, long-term morbidity and mortality remain high. The elevated long-term mortality is mainly driven by cardiac remodeling processes triggering ischemic heart failure and electric instability. Despite the new developments in pharmaco-therapy of heart failure, we still lack targeted therapies for cardiac remodeling and fibrosis. Single-cell and genomic technologies allow us to map the human heart at unprecedented resolution and allow to gain insights into cellular and molecular heterogeneity. However, these technologies rely on digested tissue and isolated cells or nuclei and thus lack spatial information. Spatial information is critical to understand tissue homeostasis and disease and can be utilized to identify disease-driving cell populations and mechanisms including cellular cross-talk. Here, we discuss recent advances in single-cell and spatial genomic technologies that give insights into cellular and molecular mechanisms of cardiac remodeling after injury and can be utilized to identify novel therapeutic targets and pave the way toward new therapies in heart failure.
    MeSH term(s) Humans ; Ventricular Remodeling ; Multiomics ; Myocardial Infarction/genetics ; Myocardial Infarction/therapy ; Myocardial Infarction/complications ; Myocardial Ischemia ; Heart Failure/genetics ; Heart Failure/therapy
    Language English
    Publishing date 2022-12-29
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.122.318333
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  8. Article ; Online: Mapping Human Cardiac Sarcoidosis by Single Nuclear and Spatial Profiling.

    Hayat, Sikander / Kramann, Rafael

    Circulation research

    2022  Volume 131, Issue 8, Page(s) 670–672

    MeSH term(s) Cardiomyopathies ; Humans ; Myocarditis ; Sarcoidosis/diagnosis
    Language English
    Publishing date 2022-09-29
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.122.321778
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  9. Article ; Online: Fibrosis in Pathology of Heart and Kidney: From Deep RNA-Sequencing to Novel Molecular Targets.

    Schreibing, Felix / Anslinger, Teresa M / Kramann, Rafael

    Circulation research

    2023  Volume 132, Issue 8, Page(s) 1013–1033

    Abstract: Diseases of the heart and the kidney, including heart failure and chronic kidney disease, can dramatically impair life expectancy and the quality of life of patients. The heart and kidney form a functional axis; therefore, functional impairment of 1 ... ...

    Abstract Diseases of the heart and the kidney, including heart failure and chronic kidney disease, can dramatically impair life expectancy and the quality of life of patients. The heart and kidney form a functional axis; therefore, functional impairment of 1 organ will inevitably affect the function of the other. Fibrosis represents the common final pathway of diseases of both organs, regardless of the disease entity. Thus, inhibition of fibrosis represents a promising therapeutic approach to treat diseases of both organs and to resolve functional impairment. However, despite the growing knowledge in this field, the exact pathomechanisms that drive fibrosis remain elusive. RNA-sequencing approaches, particularly single-cell RNA-sequencing, have revolutionized the investigation of pathomechanisms at a molecular level and facilitated the discovery of disease-associated cell types and mechanisms. In this review, we give a brief overview over the evolution of RNA-sequencing techniques, summarize most recent insights into the pathogenesis of heart and kidney fibrosis, and discuss how transcriptomic data can be used, to identify new drug targets and to develop novel therapeutic strategies.
    MeSH term(s) Humans ; RNA/metabolism ; Quality of Life ; Kidney/metabolism ; Renal Insufficiency, Chronic/metabolism ; Fibrosis ; Myofibroblasts/metabolism
    Chemical Substances RNA (63231-63-0)
    Language English
    Publishing date 2023-04-13
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.122.321761
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  10. Article ; Online: Mouse Models of Kidney Fibrosis.

    Kramann, Rafael / Menzel, Sylvia

    Methods in molecular biology (Clifton, N.J.)

    2021  Volume 2299, Page(s) 323–338

    Abstract: Chronic kidney disease (CKD) affects over 10% of the worldwide population and kidney fibrosis is a main driver of CKD and considered a therapeutic target. The mechanisms leading to kidney fibrosis are highly complexed and can be best studied in rodent ... ...

    Abstract Chronic kidney disease (CKD) affects over 10% of the worldwide population and kidney fibrosis is a main driver of CKD and considered a therapeutic target. The mechanisms leading to kidney fibrosis are highly complexed and can be best studied in rodent models. Here we describe the most commonly used kidney fibrosis models in mice, the unilateral ureteral obstruction (UUO) model and the ischemia reperfusion injury (IRI) model. Both models are easy to learn and can be applied in animals of different age, sex, and strain.
    MeSH term(s) Animals ; Biomarkers/metabolism ; Disease Models, Animal ; Female ; Fibrosis ; Humans ; Kidney/metabolism ; Kidney/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Ureteral Obstruction/metabolism ; Ureteral Obstruction/pathology
    Chemical Substances Biomarkers
    Language English
    Publishing date 2021-05-24
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1382-5_22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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