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  1. Book ; Online ; E-Book: Fibroblast growth factor 23

    White, Kenneth / Gutiérrez Rozo, Orlando / Faul, Christian

    2021  

    Author's details Edited by Christian Faul, Kenneth White, Orlando Gutierrez
    Keywords Fibroblast growth factors
    Subject code 573.4
    Language English
    Size 1 online resource (378 pages) :, illustrations
    Publisher Elsevier
    Publishing place Waltham, Massachusetts
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    ISBN 0-12-818037-4 ; 0-12-818036-6 ; 978-0-12-818037-2 ; 978-0-12-818036-5
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

    Full text online

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  2. Book ; Thesis: Der Na + /H + -Austauschinhibitor HOE642 verbessert die postischämische Erholung der Herzfunktion durch Verminderung der Ca 2 + -Überladung und Verlängerung der postischämischen Azidose

    Faul, Christian

    2002  

    Author's details vorgelegt von Christian Faul
    Language German
    Size 39 S. : Ill., graph. Darst.
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Würzburg, Diss., 2003
    HBZ-ID HT013614042
    Database Catalogue ZB MED Medicine, Health

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  3. Article ; Online: FGF23 effects on the heart-levels, time, source, and context matter.

    Faul, Christian

    Kidney international

    2018  Volume 94, Issue 1, Page(s) 7–11

    Abstract: Fibroblast growth factor 23 (FGF23) has appeared as a hormone that is massively elevated in patients with chronic kidney disease. Whether FGF23 is a risk factor that associates with cardiac pathologies and cardiovascular mortality, as suggested by a ... ...

    Abstract Fibroblast growth factor 23 (FGF23) has appeared as a hormone that is massively elevated in patients with chronic kidney disease. Whether FGF23 is a risk factor that associates with cardiac pathologies and cardiovascular mortality, as suggested by a variety of clinical studies, or additionally acts as a causative factor that induces cardiac injury, as more recently indicated by cell culture and animal studies, is under debate and the center of many ongoing experimental studies.
    MeSH term(s) Animals ; Cardiovascular Diseases ; Fibroblast Growth Factors ; Humans ; Renal Insufficiency, Chronic ; Risk Factors
    Chemical Substances Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
    Language English
    Publishing date 2018-06-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2018.03.024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Fibroblast growth factor 23, klotho and heparin.

    Thomas, S Madison / Li, Qing / Faul, Christian

    Current opinion in nephrology and hypertension

    2023  Volume 32, Issue 4, Page(s) 313–323

    Abstract: Purpose of review: Fibroblast growth factor (FGF) 23 is a bone-derived hormone that regulates phosphate and vitamin D metabolism by targeting the kidney. When highly elevated, such as in chronic kidney disease (CKD), FGF23 can also target the heart and ... ...

    Abstract Purpose of review: Fibroblast growth factor (FGF) 23 is a bone-derived hormone that regulates phosphate and vitamin D metabolism by targeting the kidney. When highly elevated, such as in chronic kidney disease (CKD), FGF23 can also target the heart and induce pathologic remodeling. Here we discuss the mechanisms that underlie the physiologic and pathologic actions of FGF23, with focus on its FGF receptors (FGFR) and co-receptors.
    Recent findings: Klotho is a transmembrane protein that acts as an FGFR co-receptor for FGF23 on physiologic target cells. Klotho also exists as a circulating variant, and recent studies suggested that soluble klotho (sKL) can mediate FGF23 effects in cells that do not express klotho. Furthermore, it has been assumed that the actions of FGF23 do not require heparan sulfate (HS), a proteoglycan that acts as a co-receptor for other FGF isoforms. However, recent studies revealed that HS can be part of the FGF23:FGFR signaling complex and modulate FGF23-induced effects.
    Summary: sKL and HS have appeared as circulating FGFR co-receptors that modulate the actions of FGF23. Experimental studies suggest that sKL protects from and HS accelerates CKD-associated heart injury. However, the in vivo relevance of these findings is still speculative.
    MeSH term(s) Humans ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/metabolism ; Glucuronidase/metabolism ; Heparin ; Receptors, Fibroblast Growth Factor ; Renal Insufficiency, Chronic/metabolism ; Animals
    Chemical Substances Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Fibroblast Growth Factors (62031-54-3) ; Glucuronidase (EC 3.2.1.31) ; Heparin (9005-49-6) ; Receptors, Fibroblast Growth Factor
    Language English
    Publishing date 2023-05-04
    Publishing country England
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1151092-4
    ISSN 1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
    ISSN (online) 1473-6543 ; 1535-3842
    ISSN 1062-4813 ; 1062-4821
    DOI 10.1097/MNH.0000000000000895
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Cardiac actions of fibroblast growth factor 23.

    Faul, Christian

    Bone

    2017  Volume 100, Page(s) 69–79

    Abstract: Fibroblast growth factors (FGF) are mitogenic signal mediators that induce cell proliferation and survival. Although cardiac myocytes are post-mitotic, they have been shown to be able to respond to local and circulating FGFs. While precise molecular ... ...

    Abstract Fibroblast growth factors (FGF) are mitogenic signal mediators that induce cell proliferation and survival. Although cardiac myocytes are post-mitotic, they have been shown to be able to respond to local and circulating FGFs. While precise molecular mechanisms are not well characterized, some FGF family members have been shown to induce cardiac remodeling under physiologic conditions by mediating hypertrophic growth in cardiac myocytes and by promoting angiogenesis, both events leading to increased cardiac function and output. This FGF-mediated physiologic scenario might transition into a pathologic situation involving cardiac cell death, fibrosis and inflammation, and eventually cardiac dysfunction and heart failure. As discussed here, cardiac actions of FGFs - with the majority of studies focusing on FGF2, FGF21 and FGF23 - and their specific FGF receptors (FGFR) and precise target cell types within the heart, are currently under experimental investigation. Especially cardiac effects of endocrine FGFs entered center stage over the past five years, as they might provide communication routes that couple metabolic mechanisms, such as bone-regulated phosphate homeostasis, or metabolic stress, such as hyperphosphatemia associated with kidney injury, with changes in cardiac structure and function. In this context, it has been shown that elevated serum FGF23 can directly tackle cardiac myocytes via FGFR4 thereby contributing to cardiac hypertrophy in models of chronic kidney disease, also called uremic cardiomyopathy. Precise characterization of FGFs and their origin and regulation of expression, and even more importantly, the identification of the FGFR isoforms that mediate their cardiac actions should help to develop novel pharmacological interventions for heart failure, such as FGFR4 inhibition to tackle uremic cardiomyopathy.
    MeSH term(s) Animals ; Cardiomyopathies/genetics ; Cardiomyopathies/metabolism ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Humans ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Fibroblast Growth Factor, Type 4/genetics ; Receptor, Fibroblast Growth Factor, Type 4/metabolism ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction/genetics ; Signal Transduction/physiology
    Chemical Substances fibroblast growth factor 23 ; Fibroblast Growth Factors (62031-54-3) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 4 (EC 2.7.10.1)
    Language English
    Publishing date 2017-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 632515-4
    ISSN 1873-2763 ; 8756-3282
    ISSN (online) 1873-2763
    ISSN 8756-3282
    DOI 10.1016/j.bone.2016.10.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 332: Show issues

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  6. Article ; Online: The bone at the intersection of kidney and heart disease.

    Campos, Isaac / Faul, Christian

    Trends in pharmacological sciences

    2021  Volume 43, Issue 2, Page(s) 84–86

    Abstract: Systemic inflammation and elevations in the hormone fibroblast growth factor 23 (FGF23) contribute to cardiac injury and death in patients with kidney disease. A new mechanistic study by Courbon et al. suggests that the bone connects the damaged kidney ... ...

    Abstract Systemic inflammation and elevations in the hormone fibroblast growth factor 23 (FGF23) contribute to cardiac injury and death in patients with kidney disease. A new mechanistic study by Courbon et al. suggests that the bone connects the damaged kidney with the damaged heart by serving as the target for a kidney-derived proinflammatory factor and responding with FGF23 secretion.
    MeSH term(s) Fibroblast Growth Factors/metabolism ; Heart Diseases ; Humans ; Hypertrophy, Left Ventricular/metabolism ; Kidney/metabolism ; Renal Insufficiency, Chronic/metabolism
    Chemical Substances Fibroblast Growth Factors (62031-54-3)
    Language English
    Publishing date 2021-12-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 282846-7
    ISSN 1873-3735 ; 0165-6147
    ISSN (online) 1873-3735
    ISSN 0165-6147
    DOI 10.1016/j.tips.2021.11.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: DACH1 as a multifaceted and potentially druggable susceptibility factor for kidney disease.

    Merscher, Sandra / Faul, Christian

    The Journal of clinical investigation

    2021  Volume 131, Issue 10

    Abstract: Kidney diseases affect more than 15% of adults in the US, yet drug development in the kidney field, when compared with that for other common diseases, has been lagging behind. Modifiers that increase the susceptibility to injury and contribute to the ... ...

    Abstract Kidney diseases affect more than 15% of adults in the US, yet drug development in the kidney field, when compared with that for other common diseases, has been lagging behind. Modifiers that increase the susceptibility to injury and contribute to the pathogenesis and progression of kidney disease include genetic and environmental factors and epigenetic mechanisms. In this issue of the JCI, Cao et al. and Doke et al. independently report the identification of a susceptibility factor called Dachshund homolog 1 (DACH1). Both groups identify an association of reduced DACH1 expression with kidney disease, using different screening approaches, studying different types of human kidney diseases, and using different experimental models, making the fact that both stumbled over the same protein very compelling. Combined, these studies highlight DACH1 as a key safeguard in the kidney, granting various cell types proper function by modulating several molecular pathways.
    MeSH term(s) Eye Proteins/genetics ; Humans ; Kidney Diseases/genetics ; Transcription Factors/genetics
    Chemical Substances DACH1 protein, human ; Eye Proteins ; Transcription Factors
    Language English
    Publishing date 2021-05-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI149043
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  8. Article ; Online: A Klotho-Derived Peptide as a Possible Novel Drug to Prevent Kidney Fibrosis.

    Isakova, Tamara / Yanucil, Christopher / Faul, Christian

    American journal of kidney diseases : the official journal of the National Kidney Foundation

    2022  Volume 80, Issue 2, Page(s) 285–288

    MeSH term(s) Fibrosis ; Glucuronidase ; Humans ; Kidney/pathology ; Kidney Diseases/pathology ; Peptides
    Chemical Substances Peptides ; Glucuronidase (EC 3.2.1.31)
    Language English
    Publishing date 2022-04-22
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 604539-x
    ISSN 1523-6838 ; 0272-6386
    ISSN (online) 1523-6838
    ISSN 0272-6386
    DOI 10.1053/j.ajkd.2022.03.006
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    Zs.MO 468: Show issues

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  9. Article ; Online: Transforming geriatric practice and workforce development: Leveraging electronic health records to train healthcare teams.

    Faul, Anna C / D'Ambrosio, Joseph G / Linzy, Katherine E / Yankeelov, Pamela A / Cotton, Samantha G / Gordon, Barbara A / Furman, Christian D

    Journal of the American Geriatrics Society

    2024  

    Language English
    Publishing date 2024-05-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80363-7
    ISSN 1532-5415 ; 0002-8614
    ISSN (online) 1532-5415
    ISSN 0002-8614
    DOI 10.1111/jgs.18928
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  10. Article ; Online: FGF23 and inflammation-a vicious coalition in CKD.

    Czaya, Brian / Faul, Christian

    Kidney international

    2019  Volume 96, Issue 4, Page(s) 813–815

    Abstract: High serum concentrations of the phosphaturic hormone, fibroblast growth factor 23 (FGF23), contribute to various tissue injuries. In chronic kidney disease, the sources of FGF23 and the stimuli that control FGF23 production differ from those in the ... ...

    Abstract High serum concentrations of the phosphaturic hormone, fibroblast growth factor 23 (FGF23), contribute to various tissue injuries. In chronic kidney disease, the sources of FGF23 and the stimuli that control FGF23 production differ from those in the physiologic scenario. Mediators of inflammation are intensively studied as potential factors that contribute to FGF23 elevations and thereby might function as drug targets to lower FGF23 levels. The present study focuses on tumor necrosis factor.
    MeSH term(s) Fibroblast Growth Factors ; Humans ; Hypophosphatemia, Familial ; Inflammation ; Renal Insufficiency, Chronic
    Chemical Substances Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
    Language English
    Publishing date 2019-09-22
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2019.05.018
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